OPHTHALMOLOGY
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RETINAL AND OPTIC NERVE DISEASES William C. Rebhun, DVM
THE NORMAL FUNDUS AND OPHTHALMOSCOPY
Before discussing equine fundic lesions, it is important to emphasize the appearance of and tremendous variations in the normal fundus that may be mistaken for abnormalities. 12, 25 The equine practitioner should practice funduscopic examination on as many horses as possible through routine ophthalmoscopy as part of the physical examination. Only after examining hundreds of normal horses, foals, and ponies can one be familiar with the range of normal variations that exist and confidently assess the equine fundus under the pressure of a soundness examination. The equine fundus is paurangiotic, as opposed to the holangiotic fundus found in most other domestic animals. Paurangiotic fundi have relatively small vessels leaving the periphery of the optic disc. These vessels radiate approximately the diameter of the optic disc into the retina peripheral to the disc. There may be 50 to 80 retinal arteries and veins that exit the optic disc in the horse. Because of this limited retinal vascular supply, the equine retina receives most of its blood supply and nutrition from the underlying vascular choroid. The fundus is divided into a dorsal tapetal zone and a ventral nontapetal zone (Fig. 1). The tapetum, a fibrous layer, is part of the choroid and provides a reflective surface that allows light entering the eye to reflect back through the retina. Horses other than color diluent or partially albinotic all have a colorful tapetum, the color of which varies with the coat color of the From the Department of Clinical Sciences, Cornell University College of Veterinary Medicine, Ithaca, New York
VETERINARY CLINICS OF NORTH AMERICA: EQUINE PRACTICE VOLUME 8 • NUMBER 3 • DECEMBER 1992
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Figure 1. Normal equine fundus.
animal. Black and dark bay horses have blue tapetums, whereas most bay horses have green-blue tapetums. Chestnut horses may have greenish or green-yellow tapetal colorations, and light-coated horses (Palominos) may have yellow tapetums. Color diluents, subalbinotic, or albinotic coat-colored horses may have areas of tapetal thinning, absence of tapetum, or absence of pigment that allow the underlying large choroidal vessel layer to be apparent. These horses usually have associated iris heterochromia or blue irides. Large choroidal vessels apparent upon fundic examination of such horses must be recognized as normal variations and not be confused with retinal hemorrhage or inflammation. A stellate network of dark spots or short bars, known as the Stars of Winslow, is present throughout the tapetum. These spots represent choroidal capillaries viewed on end as they traverse the tapetum. The normal nontapetal area is brown or dark brown in most pigmented horses because of pigment present in the pigment epithelial layer of the retina. Similar to the situation in the tapetal zone, pib.llLl:nt dilution or absence, based on coat and iris color, may lead to varying degrees of absence of pigment in this zone. Such variations in pigmentation allow ophthalmoscopic viewing of the large choroidal vessel layer. The optic disc is oval, pink-white, and located just below the junction of tapetum and nontapetum in the nontapetal zone. The optic disc is slightly ventral and temporal to the visual axis. The edges may be smooth or scalloped, based on the distribution of myelin at the disc margin. Although retinal vessels may be less concentrated in some areas of the optic disc, some vessels should be present around the entire circumference of the optic disc. The vessels originate from the
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periphery rather than the center of the optic disc and radiate approximately the diameter of one optic disc into the surrounding retina. Ophthalmoscopy can be accomplished with direct, indirect, or both types of ophthalmoscopes, depending on the veterinarian's experience and preference. 2 The author prefers direct ophthalmoscopy because of its increased magnification, direct image, and better patient cooperation. The increased size of field found with indirect lenses may be preferable to some examiners who become familiar with the reversed, inverted image obtained with this technique. If examination in complete darkness is possible, it may not be necessary to dilate the pupils for ophthalmoscopy in horses. If necessary, because of environmental lighting or miosis, short-term mydriasis can be obtained by application of several drops of 1% tropicamide (Mydriacyl, Alcon Laboratories, Fort Worth, TX). Mydriasis takes 15 to 20 minutes following application of this product. Prior to ophthalmoscopy, it is imperative to evaluate the anterior segment and determine menace response, as well as direct and consensual pupillary responses to direct light. Refer to the article by Cooley for specific details of examination techniques and normal findings. As a rule, most fundic pathology in horses exists ventral to the tapetum. 17 It is extremely important, therefore, to examine thoroughly the optic disc, peripapillary region, and nontapetum at least two disc diameters ventral to the optic disc.
RETINA Congenital Retinal Disorders
Congenital retinal lesions include colobomas, retinal detachments, and retinal abnormalities associated with multiple congenital ocular defects.2, 17, 25 Colobomas appear as blue circular or oval reflective lesions near the junction of the tapetum and nontapetum (Fig. 2). They may be located nasal or temporal to the disc and have been observed in both the tapetal and nontapetal zones. Colobomas usually are singular but rarely occur as multiple lesions in a group. The lesions usually are onefourth to one-third the optic disc diameter and appear unilaterally. Careful ophthalmoscopic examination demonstrates the lesion edges to be recessed below the level of the surrounding retina. Most horses with colobomas are asymptomatic, and the lesions are found as incidental findings. The author has examined one horse, however, which had a very large coloboma located dorsonasal to the optic disc and had a temporal field visual deficit; the horse appeared apprehensive when objects appeared in the temporal visual field. The cause of colobomas is unknown in horses, and the condition has been observed in several breeds. Congenital retinal detachments may occur unilaterally or bilaterally and cause blindness in affected eyes because they usually are complete
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Figure 2. Large coloboma located in the temporal tapetal fundus just above the tapetal/nontapetal junction.
rather than partial. Such detachments may be the only lesion present in affected eyes or may coexist with multiple congenital anomalies such as microphthalmia, cataracts, luxated lenses, aniridia, and anterior segment cleavage anomalies. Diagnosis is aided by focal light examination of the eye through the obviously dilated pupil, which allows the retina to be observed floating in the vitreous. Ophthalmoscopy confirms the diagnosis as the retina is observed in a veil-like or folded arrangement attached only at the optic disc. Frequently, the retina folds over the optic disc because the dorsal retina has fallen to the ventral vitreous, making the optic disc difficult to see. Successful treatment has not been described in foals, and the prognosis therefore is grave. Although the cause usually is unknown, developmental disorders and inheritance have been suggested. In the author's experience, the problem has been observed most commonly in Standardbred and Thoroughbred horses. Night Blindness
Night blindness (not to be confused with moon blindness, a layman's term for uveitis) occasionally is observed in foals and has been shown most likely to be an inherited trait in Appaloosa horses. 19, 30 Night blindness is similar to congenital stationary night blindness in humans, is present at birth, and persists throughout the horse's life. A spectrum of clinical signs exist, suggesting varying degrees of severity in the problem. Severely affected foals are noted shortly after birth to appear disoriented unless in direct company of the dam. These foals will star gaze and tilt the head in apparent attempts to focus on objects. They frequently have a bilateral dorsomedial strabismus. They become extremely apprehensive if forced to move in reduced or dark lighting. Depending on individual personality,
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they may become anxious and excitable, running into objects, or, alternatively, may refuse to move for fear of injury. Mildly affected foals are not suspected of having visual problems until weaned, when the mare is no longer available to guide them. Some foals are thought to be "clumsy" or awkward and a vision problem is not suspected until the yearling age. Although as yet unproved, the most severely affected horses, which show star gazing, dorsomedial strabismus, and head cocking, also may have subtle microphthalmos or refractive errors such as severe myopia as described in inherited forms of stationary night blindness in humans. 3, 13, 27, 28 These animals have some visual deficits in daylight, and these deficits are greatly exaggerated in reduced or dark lighting situations. Less severely affected horses may adjust to training and pleasure work in daylight but are disoriented, frightened, or unpredictable in dark settings. Some owners have reported having to lead the horse from pasture at night, while other owners report repeated injuries to the horse occurring during evening hours. Ophthalmologic examination of the eyes usually fails to identify lesions unless a dorsomedial strabismus is observed. Rarely, the author has observed a depression or cupping in the central region of the optic discs bilaterally in severely affected foals. Definitive diagnosis requires an electroretinogram that demonstrates a negative wave-form (the positive B-wave is absent).29 There is no treatment. A recessive inheritance pattern has been suggested in the Appaloosa horse, 3D but the cause in other breeds, such as Thoroughbreds, Standardbreds, or Paso Finos, in which the condition occurs sporadically, is unknown. Acquired Retinal Disorders
Inflammatory Retinitis and Chorioretinitis Bullet~hole Lesions. The most common fundic lesions in horses are focal or multifocal circular scars of the peripapillary and nontapetal regions. 17 These small circular lesions have a depigmented periphery and hyperpigmented central zone due to retinal pigment epithelial hypertrophy at the site of prior inflammation (Fig. 3). Bullet-hole lesions are observed in horses of all breeds and, although found primarily in adult horses, have been found in foals. The acute phase of chorioretinal inflammation that subsequently results in bullet-hole scars seldom is observed in horses. When acute lesions are found, they appear as white, soft, exudative lesions and evolve into classical bullet-hole scars over a period of 2 to 4 weeks. The only acute lesions found ophthalmoscopically by the author have been in several foals, two of which had concurrent respiratory disease. The cause of these lesions is unknown, but an association with infectious respiratory disease is suspected. Collaborative observations pre- and postinfection with equine influenza virus have not shown a relationship with this virus (Holmes 0, Rebhun WC; unpublished data, 1982), but to the author's
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Figure 3. Multiple bullet-hole scars in the nontapetal zone ventral to the optic disc.
knowledge, other respiratory pathogens have not been investigated. Roberts 23 observed similar lesions in a group of horses that had suffered infection with Streptococcus equi. Bullet-hole scars may be observed in 10% to 20% of adult horses in the northeastern United States, thus supporting relatively common exposure to the causative inflammatory insult. Ophthalmoscopic evidence of a few bullet-hole scars seldom constitutes unsoundness because vision seems unaffected in such horses. Lesions usually are bilateral but frequently vary in number in each eye. When more than 10 bullet-hole lesions are identified in an eye during ophthalmoscopy, visual testing should be done and pupillary response to direct light should be assessed carefully. Horses with 20 or more bullet-hole lesions may show decreased pupillary response to direct light, obvious visual abnormalities, or subtle visual abnormalities. Reduced vision may result in frequent corneal injuries (Fig. 4). Horses with a history of repeated corneal injury, shying, or unilateral visual defects should be examined to rule out significant numbers of bullethole lesions. The exact number and location of lesions necessary to affect vision are difficult to assess. Suffice it say that a few lesions usually are thought to be insignificant incidental findings, whereas multiple lesions (certainly 10 or more) should raise some concern relative to their cumulative damage to the retina. Generally, no other ophthalmic lesions are present in affected eyes. Treatment seldom is possible because the lesions represent scars rather than acute disease. In those rarely occurring acute cases, topical and systemic anti-inflammatory drugs would be indicated. Diffuse Chorioretinal Lesions. Diffuse chorioretinal lesions gen-
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Figure 4. Multifocal chorioretinal scars (bullet-hole scars) nasal and ventral to the optic disc in a 4year-old Thoroughbred presented because of recurrent corneal injury.
erally appear as vermiform, circular, or band-shaped lesions that are hyperreflective in the tapetal zone and depigmented in the nontapetal zone. Within the depigmented lesions in the nontapetum, areas of hyperpigmentation may be present. These lesions are uncommon and represent either widespread prior inflammatory disease or infarctive lesions with subsequent retinal degeneration and scarring. 17, 20, 25 Optic nerve atrophy may accompany these severe lesions. Similar lesions have been associated with massive blood loss in horses 7 and sometimes occur following severe skull trauma, where they probably are the result of infarction. When associated with severe skull trauma, optic nerve degeneration usually is present. The lesions may be present in one or both eyes. A careful history should be elicited from owners of these horses regarding prior illness, trauma, or vascular disease. The author has observed several blind horses affected bilaterally with these lesions but which had no antecedent history of trauma, blood loss, or infection. Subsequently, necropsy and histopathology confirmed infarctive lesions in the eyes as well as scattered infarctive lesions in the brain (Rebhun we, deLahunta A; unpublished data, 1983). No treatment is possible and affected animals are blind or have markedly reduced vision. Horizontal Band Lesions of the Nontapetal Zone. Multifocal chorioretinallesions appearing in band distribution in the nontapetal zone have been observed in horses. These lesions occur one to two disc diameters ventral to the optic disc and radiate in a horizontal fashion around the posterior pole of affected eyes. They result in markedly reduced vision or complete blindness. Individual lesions within this zone of retinal degeneration may appear as depigmented circles, ovals, or vermiform lesions (Fig. 5). Some have hyperpigmented centers. The
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Figure 5. Horizontal band distribution of chorioretinal scarring in a blind eye of a 3-year-old Standardbred.
affected zone extends from the ora ciliaris retinae nasally to the same area temporally. The cause is unknown but infarction of a major ciliary vessel has been suspected. The lesion is found unilaterally, and prior history has not been helpful in elucidating the cause in affected horses. The location of lesions emphasizes the need to examine the nontapetal area carefully ophthalmoscopically in horses having poor vision or repeated corneal injuries. Horses with this condition do not have evidence of prior ocular disease in the anterior segment. Treatment is not helpful because the lesion represents prior insult that now is inactive. Peripapillary Chorioretinitis. Peripapillary chorioretinitis and scars subsequent to this problem represent dilemmas when forecasting soundness of affected equine eyes. Active peripapillary inflammation is most commonly found in association with anterior uveitis, and this relationship is well recognized in uveitis caused by leptospirosis,14, 17,22 Onchocerca cervicalis microfilariae,l and immune-mediated uveitis of unknown etiology. Inactive peripapillary chorioretinitis or peripapillary scars suggestive of prior active inflammation require consideration of their relationship to equine uveitis. As a result, these inactive lesions frequently become topics of contention during soundness examinations. Active peripapillary chorioretinitis may be recognized ophthalmoscopically as fluffy, raised, soft or hard exudates adjacent to the optic disc. Small geographic zones of the nontapetal retina bordering the optic disc may appear pale or depigmented. Vasculitis of the retinal vessels exiting the optic disc may be present and appears as white or pale exudates surrounding affected retinal vessels. It may be difficult to differentiate pure peripapillary chorioretinitis from optic neuritis with extension into the peripapillary retina in some horses. These lesions
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are not rare but seldom are observed because most horses with active peripapillary chorioretinitis have coexisting anterior segment inflammation, making funduscopy difficult. Concurrent vitreal inflammation may further obscure fundic details. Horses with active peripapillary inflammation may develop peripapillary scars-depigmented lesions with hyperpigmented foci within them. These inactive scars have been called "butterfly" lesions because scars both nasal and temporal to the disc often assume an alar configuration (Fig. 6). In fact, however, the scar may be in any quadrant or may completely encircle the optic disc, so an alar configuration is not mandatory for their identification. Horses with active peripapillary chorioretinitis also may develop vitreoretinal adhesions subsequent to retinal vasculitis, because exudates emanating from inflamed retinal vessels may cause fibrinous vitreoretinal adhesions that eventually fibrose, causing secondary retinal elevations or detachments. 16 Active peripapillary c~orioretinitis also may be associated with inflammation, trauma, or ischemic damage to the optic nerve. In these instances, more obvious exudates and occasional frank hemorrhage may be observed ophthalmoscopically on the optic nerve and its borders. Although active lesions may be difficult to appreciate in horses with concurrent anterior uveitis, synechiae, cataracts, or vitreal inflammation, their cause in such instances quickly becomes apparent. The more difficult situation occurs when inactive peripapillary chorioretinal scars are observed in a visual eye. The retinal vessels may appear to be unaffected by the prior insult. The significance of such lesions must be assessed based on careful examination of both eyes for other lesions. The veterinarian must methodically examine the eyes for any other lesions suggestive of active or inactive uveitis. For example,
Figure 6. Butterfly type peripapillary scar nasal to the optic disc in a 12-year-old Thoroughbred. The eye was visual, and no other lesions suggestive of uveitis were identified in either eye.
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if either eye has a dark iris, synechiae, pigment that rests on the anterior lens capsule, cataract, vitreal inflammation, or unexplained peripheral corneal vascularization, uveitis should be suspected as the cause of the inactive peripapillary lesion. On the other hand, if both irises are normal and no lesions suggestive of prior ocular inflammation are identified, a unilateral peripapillary scar in a visual eye need not carry a guarded prognosis. Evaluation of the retinal vessels within the lesion also is important because regional disappearance of retinal vessels may indicate a more significant retinal lesion. Obviously, causes other than uveitis may result in peripapillary scars. If this is the only lesion found during a soundness examination, therefore, the buyer should be made aware of the finding and informed of its possible relationship to uveitis but not be informed that the animal is unsound simply because of this lesion. Inform owners or buyers that the horse may have had a prior uveitis episode but, based on the complete ophthalmic examination, there is insufficient evidence to confirm this. In fact, many horses with peripapillary scars or butterfly lesions as their only ophthalmic abnormality (usually unilaterally) never have had uveitis, nor do they develop it. Traumatic Retinal Lesions
Traumatic retinal lesions in horses-including retinal hemorrhages, retinal tears, and retinal detachments-may be associated with skull trauma or blunt ocular injuries from whips, lead shanks, or twitches. Optic nerve lesions also may be present, but discussion of these is deferred to the following section. Blunt injuries causing retinal lesions usually induce anterior segment damage to the cornea and iris. This anterior segment damage (corneal edema from endothelial damage and traumatic iritis) may obscure some fundic details. Small subretinal, intraretinal, or preretinal hemorrhages may eventually resolve with time and not interfere significantly with vision. Large retinal or vitreal hemorrhages, however, generally signal hemorrhage from the uveal tract rather than the retina and carry a guarded prognosis because of the likelihood of chorioretinal scarring and retinal degeneration in affected areas (Figs. 7 and 8). Conservative therapy with systemic nonsteroidal anti-inflammatory medication and topical therapy based on ophthalmic findings are indicated. Assuming no corneal epithelial defects are identified, topical corticosteroids and atropine should be used to control the traumatic anterior uveitis. Retinal and vitreal hemorrhages take weeks or months to resolve and therapy, at best, is supportive rather than curative. Retinal Detachments
Congenital retinal detachments occasionally are the cause of blindness in newborn foals and have been already been discussed under congenital retinal disorders. Acquired retinal detachments in adult
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Figure 7. Retinal hemorrhage following a whip injury to the eye in a 3-year-old Arabian.
horses may be associated with ocular trauma, skull trauma, or equine uveitis, and occur as delayed postsurgical complications of cataract surgery. Occasional idiopathic retinal detachments occur in older horses as well and may be associated with vitreal degenerative processes. Acquired retinal detachments may be partial or complete. Partial retinal detachments cause specific visual field deficits whereas complete detachments cause blindness and loss of direct pupillary light response. Detachments secondary to equine uveitis occur as a sequel to peripapillary vitreoretinal adhesions that cause retinal traction detachments
Figure 8. Same eye as Figure 7 showing subsequent diffuse retinal and optic nerve degeneration 6 months following the acute injury.
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Figure 9. Early-phase vitreoretinal traction band detachments of the retina in the peripapillary region secondary to uveitis in a 6-year-old Standardbred horse.
(Fig. 9). Vitreoretinal traction detachments progress to complete detachment because of vitreal fibrosis. Generally, retinal detachments occur months to years after the initial uveitis and occasionally develop in uveitis-affected eyes that appear to be currently free of anterior segment inflammation. Such detachments may be recognized by a sunburst appearance of multiple radiatory retinal veils attached near the optic disc (Fig. 10). Although
Figure 10. Complete retinal detachment.
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treatment of partial retinal detachment is possible theoretically, on a practical basis, therapy is unlikely to be successful.
OPTIC NERVE Congenital Lesions
Congenital lesions of the optic nerve are extremely rare in horses. Gelatt8 reported one foal with bilateral optic nerve hypoplasia, and Rubin25 refers to a foal with congenital optic nerve atrophy (vascular atrophy and a normal optic disc). If in utero inflammation had been present in these cases, peripapillary lesions suggestive of prior inflammation would be present. Optic nerve hypoplasia may be misdiagnosed in foals with multiple congenital ocular anomalies or luxated lenses, because the optic disc appears smaller ophthalmoscopically because of optical changes in the eye caused by the anomalies. Colobomas of the central optic disc occasionally have been observed in Appaloosas affected with night blindness. These lesions are subtle and are not a characteristic finding in night-blind Appaloosas, given that the fundus typically appears normal in these horses.
Acquired Disorders
Traumatic Damage
Traumatic damage to the optic nerve is associated with skull trauma in horses that fall over backwards or rise up in starting gates, trailers, or stalls with low ceilings. 7, 11, 18 Retrobulbar damage to the optic nerve may occur within the optic canals or at the point of exit from the optic foramen. Although more common as a unilateral lesion, occasional bilateral lesions occur. The result is partial or complete visual loss in the affected eye within 24 hours of injury. Direct pupillary light response is reduced or absent. Ophthalmoscopic lesions, including edema or hemorrhage (Fig. 11), may be present within 24 to 48 hours of the injury, but are not present in many horses because of the retrobulbar nature of the injury. Similar to retrobulbar optic nerve damage in other species, the optic disc may appear normal but the diagnosis is made because "the patient sees nothing and the doctor sees nothing." Edema and hemorrhage in the retrobulbar portion of the affected optic nerve may be most prominent within the bony confines of the optic canals. Because of the nature of horses, severe skull trauma may cause a whiplash-type snapping injury at the cranial aspect of the optic canal, thereby causing extensive physical and inflammatory damage at this point. Ophthalmoscopy immediately postinjury may be difficult in horses that have extensive periorbital trauma, eyelid swelling, or orbital fractures.
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Figure 11. Hemorrhage overlying the optic disc and around one retinal vessel dorsal to the disc in a horse that had suffered skull trauma 24 hours earlier.
Treatment should be intensive and immediate if vision or pupillary light reflexes are reduced. Intravenous dimethylsulfoxide (1 g/kg body weight), systemic nonsteroidal anti-inflammatory drugs, and judicious doses of systemic corticosteroids should be employed and repeated as necessary. As always, the relative value of systemic corticosteroids in this instance must be weighed against their potential dangers (i.e., laminitis, enteritis). Successful therapy should restore pupillary and visual function within 72 hours. Lack of response after this time signals permanent optic nerve damage. Permanent damage eventually leads to an atrophic appearance to the optic disc after several weeks or months due to degeneration of myelinated optic nerve fibers (Fig. 12). Some horses will have partial return of vision with subsequent regional pallor or vascular loss in the optic disc. Infarction
Optic nerve infarction occurs sporadically and may be associated with vascular insults,15 multifocal central nervous system infarction, trauma, or sepsis, or may occur following surgical ligation of carotid artery branches for guttural pouch mycosis. The best opportunity to study ischemic optic nerve lesions has occurred in recent years because of surgical techniques employed for treatment of guttural pouch mycosis. 4 , 5, 6, 10 Ligation or occlusion of the common carotid artery or its branches occasionally results in ipsilateral blindness within 1 week of surgery. A dilated, nonresponsive pupil and complete blindness occur
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Figure 12. Complete optic atrophy subsequent to prior traumatic optic neuropathy in a horse.
in these horses. The author has had the opportunity to follow three such horses in Cornell's teaching hospital. Initial ophthalmoscopic examination finds a very subtle optic disc pallor, although the retinal vessels are still apparent. Within 3 to 5 days, the appearance of the disc changes and perivascular edema typical of venous outflow disturbance are observed. These changes seem to indicate an initial arterial infarction with later venous thrombosis or venous outflow disturbance. Eventual optic atrophy with vascular loss occurs but is not appreciable ophthalmoscopically for weeks following the initial infarction. The prognosis is extremely guarded and, to date, the author has not restored vision in any horse afflicted with this condition, despite symptomatic therapy. If trauma and sepsis are ruled out, the rare idiopathic instances of optic nerve infarction lesions associated with multifocal central nervous system infarction can only be diagnosed absolutely by histopathology following necropsy. Inflammatory Optic Nerve Lesions
Inflammatory optic neuritis in horses most commonly is observed in association with equine uveitis but also may occur rarely in septicemia and multifocal central nervous system infections due to bacterial and protozoan organisms. Optic neuritis in equine uveitis patients may occur alone or in conjunction \vith retinal vasculitis and peripapillary chorioretinitis. 25 These lesions have been observed in uveitis due to leptospirosis,14 Onchocerca cervicalis larvae, 1 and idiopathic immunemediated causes. Papillitis, retinal vasculitis characterized by gray or
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white exudates following the course of retinal vessels, and fluffy peripapillary lesions that appear depigmented may be observed. Short of histopathology, it is difficult to differentiate these lesions from a pure peripapillary chorioretinitis, as previously discussed. One important differentiating sign, however, is the presence or absence of vision. Uveitis patients showing true optic neuritis tend to be blind, while those with only peripapillary chorioretinitis tend to be visual, albeit compromised visually. As in the discussion of retinal inflammation, anterior segment lesions may partially obscure fundic details, thereby further interfering with ophthalmoscopic differentiation of the posterior segment lesions. Septic lesions of the optic nerve have a more malignant course and initially appear as optic disc inflammation characterized by hard or soft exudates, hemorrhage, or edema (Fig. 13). Septic uveitis or endophthalmitis is the feared and usual sequela as the vitreous subsequently is infected. Such lesions have been observed rarely in septicemic foals and adult horses having septicemia, endocarditis,24 or multifocal protozoan encephalomyelitis. Regarding protozoan organisms, both Toxoplasma gondii and Sarcocystis neurona should be considered as possible causative agents, but both rarely cause ophthalmic manifestations in the horse. Bacterial organisms include Streptococcus spp., Actinobacillus equuli, and Rhodococcus equi. Septic lesions usually are observed in fulminating septic situations and carry a grave prognosis for life, in the author's experience. Other causes of optic neuritis are rare. Borna disease, or viral encephalomyelitis, is an exotic viral disease capable of causing optic neuritis in horses but is not seen in the United States. 25 Another inflammatory optic neuritis, termed exudative optic neuritis, has been
Figure 13. Optic nerve septic inflammation, which subsequently progressed to endophthalmitis in a horse having endocarditis.
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recognized in Europe 25 and occasionally in the United States. Hard and soft exudate radiates from the optic disc and is raised into the vitreous, creating a dramatic lesion associated with acute blindness. Hemorrhage also may be evident, radiating from the optic nerve. The cause of this condition is unknown. Sepsis and prior trauma should be ruled out through history, physical examination, and necessary ancillary procedures. Treatment is unlikely to be successful and would be symptomatic, at best. Proliferative Optic Neuropathy
This lesion usually is found as a unilateral incidental finding in aged horses (over 15 years of age). The author has observed the lesion in one horse that was only 6 years of age, however. A pedunculated white mass attached to the periphery of the optic disc protrudes into the vitreous humor (Fig. 14). Much debate exists as to the exact cell origin and components of proliferative optic neuropathy. One report considered the lesions as astrocytoma, 9 whereas another suggested that the foamy cells identified histologically resembled a lipid storage such as observed in human xanthomatosis. 25, 26 The author recently collaborated on a study with histopathologic and electron microscopy of a lesion that suggested a Schwann cell derivation of the granular cells. 21 In any event, the lesions generally are benign and are incidental findings. Larger proliferative optic neuropathic lesions may be observed to wave about in the vitreous when the horse's eye moves. Although generally benign, the lesions do continue to enlarge over months or years. The author has examined two horses over 20 years of
Figure 14. Proliferative optic neuropathy.
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age that had such large proliferative lesions that behavior and vision were affected. The horses became apprehensive on the ipsilateral side. Ophthalmoscopy revealed proliferative optic neuropathies nearly as large as the optic disc itself-large enough to wave noticeably in the vitreous, casting a shadow on the retina ventral to the lesion. Because the lesions generally are benign, no treatment usually is indicated and the author knows of no surgical attempt at removal, to date.
THE VITREOUS Congenital Disorders
Congenital vitreal lesions in the horse are limited to persistent hyaloid arteries and remnants thereof. The hyaloid artery and arterial system (tunica vasculosa lentis) around the lens normally disappear before birth in foals. Persistent hyaloid arteries are less common in newborn foals than in most other domestic neonates but occasionally are observed. A distinct linear structure traversing the vitreous from the optic disc to the axial posterior cortex of the lens will be apparent upon ophthalmoscopy when a hyaloid artery remnant persists. Rarely, this vessel may still contain blood, as it does in the embryonic eye, but usually only a vascular remnant that appears gray-white or dark in color is found. Persistent hyaloid artery remnants found in newborn foals generally disappear by 3 to 4 months of age. The only clinical concern generated by this entity is possible damage to the axial posterior lens capsule and subsequent focal cataract formation at this site. If a cataract is caused at this site, the potential for further cataract formation may exist. Fortunately, these axial capsular cataracts seldom progress and tend to remain stable for the horse's entire life.
Inflammatory Disorders
Vitreal inflammation (vitreitis, vitritis) is extremely common in horses affected with uveitis. Inflammatory cells and fibrin from the inflamed uveal tract may cause diffuse or focal vitreal opacities. Fibrin and porphyrin metabolites that ooze into the vitreous cause a yellowgreen appearance when focal light is directed through the pupil of some horses with uveitis. This color and a generally dull or reduced tapetal reflection signal vitreal inflammation. Clumps, veils, or floating accumulations of vitreal debris may be observed in uveitis-affected eyes and these accumulations generally are mobile when the eye moves. Heavy vitreal accumulations greatly interfere with the horse's vision and obscure fundic details during ophthalmic examination. Severe vitreal inflammation promotes syneresis in the vitreous such that the normal vitreous gel separates into liquid and solid protein (inflamma-
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tory cells and vitreal protein) components. Thus, further mobility is granted the floating debris as the normal vitreous gel liquifies. Vitreal inflammation also may contribute to lenticular metabolic disorders resulting in cataract formation in uveitis patients. Intensive therapies with anti-inflammatory drugs that establish levels in the vitreous are indicated when treating uveitis patients with extensive vitritis. These might include systemic corticosteroids, subconjunctival repository corticosteroid injections, and topical corticosteroids (i.e., prednisolone acetate preparations) that penetrate the cornea sufficiently to establish significant intraocular levels. The prognosis for vitritis is guarded because vitreal degeneration induced by the inflammation is irreversible to some degree. In addition, products (cells, proteins) deposited in the vitreous are "trapped" in this cavity, given the poor resorption capabilities of the posterior segment. Vitreoretinal adhesions also may develop as fibrin strands contract and fibrose, predisposing to retinal detachments. Septic vitritis of embolic origin also is an extremely serious problem since treatment by other than vitrectomy plus intensive systemic, subconjunctival, and topical antibiotic therapy is unlikely to prevent endophthalmitis or panophthalmitis. Septic vitritis is observed occasionally in septicemic foals, and a dense inflammatory cloud is observed in the vitreous. Septic uveitis typically coexists. A grave prognosis is indicated since overwhelming septicemia is the usual cause. The only successful cases managed by the author have been Streptococcal in origin, where systemic and topical chloramphenicol was successful. Most neonatal septicemias are due to gram-negative bacteria (Escherichia coli, Klebsiella, Salmonella, Actinobacillus equuli), however, and vitritis due to these organisms is more difficult to resolve than Streptococcal vitritis.
Vitreal Degeneration
The simplest and most common form of vitreal degeneration is the vitreal floater. Most horses over 6 years of age have some vitreal floaters, as do most adult people. Insignificant or incidental vitreal floaters first appear as refractile mobile strands that can best be observed during ophthalmoscopy and retroillumination using the "0" diopter setting of the direct ophthalmoscope at a distance of 12 to 18 inches (30.5 to 45.7 cm) from the eye. While allowing the horse's eye to move normally, the examiner looks through the ophthalmoscope to highlight these floaters against the colorful tapetal background (Fig. 15). The importance of vitreal floaters is the occasionally real, but usually false, syndrome of the "fly-eyed" horse that appears to shy for no apparent reason. Ruling out extensive vitreal floaters is part of the examination performed on horses with this complaint as well as in horses having the major medical dilemma known as "head shaking." Vitreal floaters seldom are the cause of these conditions, but there are
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Figure 15. Large single vitreal floater highlighted against the colorful tapetal background in an equine eye.
rare instances in which exhaustive medical workups turn up no other reason for the problem. In the author's experience, vitreal floaters causing behavioral changes usually are observed at a rate of one case every 1 or 2 years. More extensive vitreal degeneration in middle-aged or older horses usually is due to vitreal syneresis with fractionation of the vitreous gel into solid and liquid components. This may take several forms, the simplest of which is the development of extensive vitreal strands and floaters that appear dark rather than refractile when viewed against the colorful tapetal background. Most horses with this condition are asymptomatic but, rarely, an animal may show visual or behavioral disturbance. Other types of vitreal degeneration are less common in horses. Asteroid hyalosis or cholesterolosis bulbi appears in horses in a fashion similar to other species. Stationary crystals, thought to be cholesterol or calcium-lipid material, are scattered diffusely through the vitreous like a constellation of stars. The crystals are small (1-2 mm) and refract light during focal light examination of the posterior pole. Asteroid hyalosis in horses usually is an incidental finding that does not appear to affect vision. It is found in older horses that generally are not in performance, so exact statements as to its effects on vision are difficult to interpret. Synchysis scintillans is another degenerative condition of the vitreous occasionally observed in older horses. Vitreal syneresis or liquefaction has occurred in these horses, and the solid component of the vitreous has coalesced into crystalline material that floats and moves freely during normal ocular movements. The appearance has been compared to a snow-scene paperweight in which the particles slowly
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filter through the fluid when the paperweight is moved or inverted. This condition usually is an incidental finding and, similar to asteroid hyalosis, affected horses appear to be visual.
References 1. Cello RM: Ocular onchocerciasis in the horse. Equine Vet J 3:148-154, 1971 2. Crispin SM, Matthews AG, Parker J: The equine fundus, I: Examination, embryology, structure and function. Equine Vet J (suppl)10:42-49, 1990 3. DerKaloustian V, Baghdassarian SA: The autosomal recessive variety of congenital stationary night-blindness with myopia. J Med Genet 9(67):67-69, 1972 4. Freeman DE, Donawick WJ: Occlusion of the internal carotid artery in the horse by means of a balloon-tipped catheter: Evaluation of a method designed to prevent epistaxis caused by guttural pouch mycosis. J Am Vet Med Assoc 176(3):232-235, 1980 5. Freeman DE, Ross MW, Donawick WJ: "Steal phenomenon" proposed as the cause of blindness after arterial occlusion for treatment of guttural pouch mycosis in horses. J Am Vet Med Assoc 197(7):811-812, 1990 6. Freeman DE, Ross MW, Donawick WJ, et al: Occlusion of the external carotid and maxillary arteries in the horse to prevent hemorrhage from guttural pouch mycosis. Vet Surg 18(1):39-47, 1989 7. Gelatt KN: Neuroretinopathy in horses. J Equine Med Surg 3(2):91-96, 1979 8. Gelatt KN, Leipold HW, Coffman JR: Bilateral optic nerve hypoplasia in a colt. J Am Vet Med Assoc 155(4):627-631, 1969 9. Gelatt K, Leipold H, Finocchio E, et al: Optic disc astrocytoma in a horse. Can Vet J 12:53-55, 1971 10. Hardy J, Robertson JT, Wilkie DA: Ischemic optic neuropathy and blindness after arterial occlusion and treatment of guttural pouch mycosis in two horses. J Am Vet Med Assoc 196:1631-1634, 1961 11. Martin L, Kaswan R, Chapman W: Four cases of traumatic optic nerve blindness in the horse. Equine Vet J 18(2):133-137, 1986 12. Matthews AG, Crispin SM, Parker J: The equine fundus, II: Normal anatomical variants and colobomata. Equine Vet J (suppl)10:50-54, 1990 13. Merin S, Rose H, Auerbach E, et al: Syndrome of congenital high myopia with nyctalopia. Am J Ophthalmol 780(4):541-547, 1970 14. Morter RL, Williams RD, Bolte H, et al: Equine leptospirosis. J Am Vet Med Assoc 155:436-442, 1969 15. Platt H, Barnett KC, Barry DR, et al: Degenerative lesions of the optic nerve in Equidae. Equine Vet J (suppl)2:91-97, 1983 16. Rebhun WC: Diagnosis and treatment of equine uveitis. J Am Vet Med Assoc 175(8):803-808, 1979 17. Rebhun WC: Equine retinal lesions and retinal detachments. Equine Vet J (suppl)2:8690, 1983 18. Rebhun WC: Traumatic optic neuropathy: How to prevent permanent blindness. Vet Med Small Anim Clin April:350-353, 1986 19. Rebhun WC, Loew ER, Riis RC: Clinical manifestation of night blindness in the Appaloosa horse. Compend Contin Educ Pract Vet 6(2):S103-5106, 1984 20. Riis RC: Equine ophthalmology. In Gelatt KN (ed): Textbook of Veterinary Ophthalmology. Philadelphia, Lea & Febiger, 1981, pp 569-605 21. Riis RC, Rebhun WC: Proliferative optic neuropathy in a horse caused by a granular cell tumour. Equine Vet J (suppl)10:69-72, 1990 22. Roberts 5J: Sequelae of leptospirosis in horses on a small farm. J Am Vet Med Assoc 133:189-194, 1958 23. Roberts SR: Chorioretinitis in a band of horses. J Am Vet Med Assoc 158(12):20432046, 1971
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24. Ross CE, Rebhun WC, Dietze AE, et al: Case report: Endocarditis and optic neuritis in a Quarter Horse mare. Compend Contin Educ Pract Vet 9(4):451-454, 1987 25. Rubin LF: Atlas of Veterinary Ophthalmoscopy. Philadelphia, Lea & Febiger, 1974 26. Saunders LZ, Bistner 51, Rubin LF: Proliferative optic neuropathy in horses. Vet Pathol 9:368-378, 1972 27. Syversen D: Sex-linked essential nyctalopia in a Norwegian family. Acta Ophthalmol 52(1):145-149, 1974 28. Volker-Dieben HJ, Went LN: Ophthalmologic and genetic study of a family with nyctalopia and myopia. Ophthalmologica 171:358-359, 1975 29. Witzel DA, Joyce JR, Smith EL: Electroretinography of congenital night blindness in the Appaloosa filly. J Equine Med Surg 1(6):226-229, 1977 30. Witzel DA, Riis RC, Rebhun WC, et al: Night blindness in the Appaloosa: A sibling occurrence. J Equine Med Surg 1(11):383-386, 1977
Address reprint requests to William C. Rebhun, DVM Department of Clinical Sciences Cornell University College of Veterinary Medicine Ithaca, NY 14853
0749-0739/92 $0.00 + .20
RETINAL AND OPTIC NERVE DISEASES William C. Rebhun, DVM
THE NORMAL FUNDUS AND OPHTHALMOSCOPY
Before discussing equine fundic lesions, it is important to emphasize the appearance of and tremendous variations in the normal fundus that may be mistaken for abnormalities. 12, 25 The equine practitioner should practice funduscopic examination on as many horses as possible through routine ophthalmoscopy as part of the physical examination. Only after examining hundreds of normal horses, foals, and ponies can one be familiar with the range of normal variations that exist and confidently assess the equine fundus under the pressure of a soundness examination. The equine fundus is paurangiotic, as opposed to the holangiotic fundus found in most other domestic animals. Paurangiotic fundi have relatively small vessels leaving the periphery of the optic disc. These vessels radiate approximately the diameter of the optic disc into the retina peripheral to the disc. There may be 50 to 80 retinal arteries and veins that exit the optic disc in the horse. Because of this limited retinal vascular supply, the equine retina receives most of its blood supply and nutrition from the underlying vascular choroid. The fundus is divided into a dorsal tapetal zone and a ventral nontapetal zone (Fig. 1). The tapetum, a fibrous layer, is part of the choroid and provides a reflective surface that allows light entering the eye to reflect back through the retina. Horses other than color diluent or partially albinotic all have a colorful tapetum, the color of which varies with the coat color of the From the Department of Clinical Sciences, Cornell University College of Veterinary Medicine, Ithaca, New York
VETERINARY CLINICS OF NORTH AMERICA: EQUINE PRACTICE VOLUME 8 • NUMBER 3 • DECEMBER 1992
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Figure 1. Normal equine fundus.
animal. Black and dark bay horses have blue tapetums, whereas most bay horses have green-blue tapetums. Chestnut horses may have greenish or green-yellow tapetal colorations, and light-coated horses (Palominos) may have yellow tapetums. Color diluents, subalbinotic, or albinotic coat-colored horses may have areas of tapetal thinning, absence of tapetum, or absence of pigment that allow the underlying large choroidal vessel layer to be apparent. These horses usually have associated iris heterochromia or blue irides. Large choroidal vessels apparent upon fundic examination of such horses must be recognized as normal variations and not be confused with retinal hemorrhage or inflammation. A stellate network of dark spots or short bars, known as the Stars of Winslow, is present throughout the tapetum. These spots represent choroidal capillaries viewed on end as they traverse the tapetum. The normal nontapetal area is brown or dark brown in most pigmented horses because of pigment present in the pigment epithelial layer of the retina. Similar to the situation in the tapetal zone, pib.llLl:nt dilution or absence, based on coat and iris color, may lead to varying degrees of absence of pigment in this zone. Such variations in pigmentation allow ophthalmoscopic viewing of the large choroidal vessel layer. The optic disc is oval, pink-white, and located just below the junction of tapetum and nontapetum in the nontapetal zone. The optic disc is slightly ventral and temporal to the visual axis. The edges may be smooth or scalloped, based on the distribution of myelin at the disc margin. Although retinal vessels may be less concentrated in some areas of the optic disc, some vessels should be present around the entire circumference of the optic disc. The vessels originate from the
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periphery rather than the center of the optic disc and radiate approximately the diameter of one optic disc into the surrounding retina. Ophthalmoscopy can be accomplished with direct, indirect, or both types of ophthalmoscopes, depending on the veterinarian's experience and preference. 2 The author prefers direct ophthalmoscopy because of its increased magnification, direct image, and better patient cooperation. The increased size of field found with indirect lenses may be preferable to some examiners who become familiar with the reversed, inverted image obtained with this technique. If examination in complete darkness is possible, it may not be necessary to dilate the pupils for ophthalmoscopy in horses. If necessary, because of environmental lighting or miosis, short-term mydriasis can be obtained by application of several drops of 1% tropicamide (Mydriacyl, Alcon Laboratories, Fort Worth, TX). Mydriasis takes 15 to 20 minutes following application of this product. Prior to ophthalmoscopy, it is imperative to evaluate the anterior segment and determine menace response, as well as direct and consensual pupillary responses to direct light. Refer to the article by Cooley for specific details of examination techniques and normal findings. As a rule, most fundic pathology in horses exists ventral to the tapetum. 17 It is extremely important, therefore, to examine thoroughly the optic disc, peripapillary region, and nontapetum at least two disc diameters ventral to the optic disc.
RETINA Congenital Retinal Disorders
Congenital retinal lesions include colobomas, retinal detachments, and retinal abnormalities associated with multiple congenital ocular defects.2, 17, 25 Colobomas appear as blue circular or oval reflective lesions near the junction of the tapetum and nontapetum (Fig. 2). They may be located nasal or temporal to the disc and have been observed in both the tapetal and nontapetal zones. Colobomas usually are singular but rarely occur as multiple lesions in a group. The lesions usually are onefourth to one-third the optic disc diameter and appear unilaterally. Careful ophthalmoscopic examination demonstrates the lesion edges to be recessed below the level of the surrounding retina. Most horses with colobomas are asymptomatic, and the lesions are found as incidental findings. The author has examined one horse, however, which had a very large coloboma located dorsonasal to the optic disc and had a temporal field visual deficit; the horse appeared apprehensive when objects appeared in the temporal visual field. The cause of colobomas is unknown in horses, and the condition has been observed in several breeds. Congenital retinal detachments may occur unilaterally or bilaterally and cause blindness in affected eyes because they usually are complete
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Figure 2. Large coloboma located in the temporal tapetal fundus just above the tapetal/nontapetal junction.
rather than partial. Such detachments may be the only lesion present in affected eyes or may coexist with multiple congenital anomalies such as microphthalmia, cataracts, luxated lenses, aniridia, and anterior segment cleavage anomalies. Diagnosis is aided by focal light examination of the eye through the obviously dilated pupil, which allows the retina to be observed floating in the vitreous. Ophthalmoscopy confirms the diagnosis as the retina is observed in a veil-like or folded arrangement attached only at the optic disc. Frequently, the retina folds over the optic disc because the dorsal retina has fallen to the ventral vitreous, making the optic disc difficult to see. Successful treatment has not been described in foals, and the prognosis therefore is grave. Although the cause usually is unknown, developmental disorders and inheritance have been suggested. In the author's experience, the problem has been observed most commonly in Standardbred and Thoroughbred horses. Night Blindness
Night blindness (not to be confused with moon blindness, a layman's term for uveitis) occasionally is observed in foals and has been shown most likely to be an inherited trait in Appaloosa horses. 19, 30 Night blindness is similar to congenital stationary night blindness in humans, is present at birth, and persists throughout the horse's life. A spectrum of clinical signs exist, suggesting varying degrees of severity in the problem. Severely affected foals are noted shortly after birth to appear disoriented unless in direct company of the dam. These foals will star gaze and tilt the head in apparent attempts to focus on objects. They frequently have a bilateral dorsomedial strabismus. They become extremely apprehensive if forced to move in reduced or dark lighting. Depending on individual personality,
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they may become anxious and excitable, running into objects, or, alternatively, may refuse to move for fear of injury. Mildly affected foals are not suspected of having visual problems until weaned, when the mare is no longer available to guide them. Some foals are thought to be "clumsy" or awkward and a vision problem is not suspected until the yearling age. Although as yet unproved, the most severely affected horses, which show star gazing, dorsomedial strabismus, and head cocking, also may have subtle microphthalmos or refractive errors such as severe myopia as described in inherited forms of stationary night blindness in humans. 3, 13, 27, 28 These animals have some visual deficits in daylight, and these deficits are greatly exaggerated in reduced or dark lighting situations. Less severely affected horses may adjust to training and pleasure work in daylight but are disoriented, frightened, or unpredictable in dark settings. Some owners have reported having to lead the horse from pasture at night, while other owners report repeated injuries to the horse occurring during evening hours. Ophthalmologic examination of the eyes usually fails to identify lesions unless a dorsomedial strabismus is observed. Rarely, the author has observed a depression or cupping in the central region of the optic discs bilaterally in severely affected foals. Definitive diagnosis requires an electroretinogram that demonstrates a negative wave-form (the positive B-wave is absent).29 There is no treatment. A recessive inheritance pattern has been suggested in the Appaloosa horse, 3D but the cause in other breeds, such as Thoroughbreds, Standardbreds, or Paso Finos, in which the condition occurs sporadically, is unknown. Acquired Retinal Disorders
Inflammatory Retinitis and Chorioretinitis Bullet~hole Lesions. The most common fundic lesions in horses are focal or multifocal circular scars of the peripapillary and nontapetal regions. 17 These small circular lesions have a depigmented periphery and hyperpigmented central zone due to retinal pigment epithelial hypertrophy at the site of prior inflammation (Fig. 3). Bullet-hole lesions are observed in horses of all breeds and, although found primarily in adult horses, have been found in foals. The acute phase of chorioretinal inflammation that subsequently results in bullet-hole scars seldom is observed in horses. When acute lesions are found, they appear as white, soft, exudative lesions and evolve into classical bullet-hole scars over a period of 2 to 4 weeks. The only acute lesions found ophthalmoscopically by the author have been in several foals, two of which had concurrent respiratory disease. The cause of these lesions is unknown, but an association with infectious respiratory disease is suspected. Collaborative observations pre- and postinfection with equine influenza virus have not shown a relationship with this virus (Holmes 0, Rebhun WC; unpublished data, 1982), but to the author's
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Figure 3. Multiple bullet-hole scars in the nontapetal zone ventral to the optic disc.
knowledge, other respiratory pathogens have not been investigated. Roberts 23 observed similar lesions in a group of horses that had suffered infection with Streptococcus equi. Bullet-hole scars may be observed in 10% to 20% of adult horses in the northeastern United States, thus supporting relatively common exposure to the causative inflammatory insult. Ophthalmoscopic evidence of a few bullet-hole scars seldom constitutes unsoundness because vision seems unaffected in such horses. Lesions usually are bilateral but frequently vary in number in each eye. When more than 10 bullet-hole lesions are identified in an eye during ophthalmoscopy, visual testing should be done and pupillary response to direct light should be assessed carefully. Horses with 20 or more bullet-hole lesions may show decreased pupillary response to direct light, obvious visual abnormalities, or subtle visual abnormalities. Reduced vision may result in frequent corneal injuries (Fig. 4). Horses with a history of repeated corneal injury, shying, or unilateral visual defects should be examined to rule out significant numbers of bullethole lesions. The exact number and location of lesions necessary to affect vision are difficult to assess. Suffice it say that a few lesions usually are thought to be insignificant incidental findings, whereas multiple lesions (certainly 10 or more) should raise some concern relative to their cumulative damage to the retina. Generally, no other ophthalmic lesions are present in affected eyes. Treatment seldom is possible because the lesions represent scars rather than acute disease. In those rarely occurring acute cases, topical and systemic anti-inflammatory drugs would be indicated. Diffuse Chorioretinal Lesions. Diffuse chorioretinal lesions gen-
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Figure 4. Multifocal chorioretinal scars (bullet-hole scars) nasal and ventral to the optic disc in a 4year-old Thoroughbred presented because of recurrent corneal injury.
erally appear as vermiform, circular, or band-shaped lesions that are hyperreflective in the tapetal zone and depigmented in the nontapetal zone. Within the depigmented lesions in the nontapetum, areas of hyperpigmentation may be present. These lesions are uncommon and represent either widespread prior inflammatory disease or infarctive lesions with subsequent retinal degeneration and scarring. 17, 20, 25 Optic nerve atrophy may accompany these severe lesions. Similar lesions have been associated with massive blood loss in horses 7 and sometimes occur following severe skull trauma, where they probably are the result of infarction. When associated with severe skull trauma, optic nerve degeneration usually is present. The lesions may be present in one or both eyes. A careful history should be elicited from owners of these horses regarding prior illness, trauma, or vascular disease. The author has observed several blind horses affected bilaterally with these lesions but which had no antecedent history of trauma, blood loss, or infection. Subsequently, necropsy and histopathology confirmed infarctive lesions in the eyes as well as scattered infarctive lesions in the brain (Rebhun we, deLahunta A; unpublished data, 1983). No treatment is possible and affected animals are blind or have markedly reduced vision. Horizontal Band Lesions of the Nontapetal Zone. Multifocal chorioretinallesions appearing in band distribution in the nontapetal zone have been observed in horses. These lesions occur one to two disc diameters ventral to the optic disc and radiate in a horizontal fashion around the posterior pole of affected eyes. They result in markedly reduced vision or complete blindness. Individual lesions within this zone of retinal degeneration may appear as depigmented circles, ovals, or vermiform lesions (Fig. 5). Some have hyperpigmented centers. The
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Figure 5. Horizontal band distribution of chorioretinal scarring in a blind eye of a 3-year-old Standardbred.
affected zone extends from the ora ciliaris retinae nasally to the same area temporally. The cause is unknown but infarction of a major ciliary vessel has been suspected. The lesion is found unilaterally, and prior history has not been helpful in elucidating the cause in affected horses. The location of lesions emphasizes the need to examine the nontapetal area carefully ophthalmoscopically in horses having poor vision or repeated corneal injuries. Horses with this condition do not have evidence of prior ocular disease in the anterior segment. Treatment is not helpful because the lesion represents prior insult that now is inactive. Peripapillary Chorioretinitis. Peripapillary chorioretinitis and scars subsequent to this problem represent dilemmas when forecasting soundness of affected equine eyes. Active peripapillary inflammation is most commonly found in association with anterior uveitis, and this relationship is well recognized in uveitis caused by leptospirosis,14, 17,22 Onchocerca cervicalis microfilariae,l and immune-mediated uveitis of unknown etiology. Inactive peripapillary chorioretinitis or peripapillary scars suggestive of prior active inflammation require consideration of their relationship to equine uveitis. As a result, these inactive lesions frequently become topics of contention during soundness examinations. Active peripapillary chorioretinitis may be recognized ophthalmoscopically as fluffy, raised, soft or hard exudates adjacent to the optic disc. Small geographic zones of the nontapetal retina bordering the optic disc may appear pale or depigmented. Vasculitis of the retinal vessels exiting the optic disc may be present and appears as white or pale exudates surrounding affected retinal vessels. It may be difficult to differentiate pure peripapillary chorioretinitis from optic neuritis with extension into the peripapillary retina in some horses. These lesions
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are not rare but seldom are observed because most horses with active peripapillary chorioretinitis have coexisting anterior segment inflammation, making funduscopy difficult. Concurrent vitreal inflammation may further obscure fundic details. Horses with active peripapillary inflammation may develop peripapillary scars-depigmented lesions with hyperpigmented foci within them. These inactive scars have been called "butterfly" lesions because scars both nasal and temporal to the disc often assume an alar configuration (Fig. 6). In fact, however, the scar may be in any quadrant or may completely encircle the optic disc, so an alar configuration is not mandatory for their identification. Horses with active peripapillary chorioretinitis also may develop vitreoretinal adhesions subsequent to retinal vasculitis, because exudates emanating from inflamed retinal vessels may cause fibrinous vitreoretinal adhesions that eventually fibrose, causing secondary retinal elevations or detachments. 16 Active peripapillary c~orioretinitis also may be associated with inflammation, trauma, or ischemic damage to the optic nerve. In these instances, more obvious exudates and occasional frank hemorrhage may be observed ophthalmoscopically on the optic nerve and its borders. Although active lesions may be difficult to appreciate in horses with concurrent anterior uveitis, synechiae, cataracts, or vitreal inflammation, their cause in such instances quickly becomes apparent. The more difficult situation occurs when inactive peripapillary chorioretinal scars are observed in a visual eye. The retinal vessels may appear to be unaffected by the prior insult. The significance of such lesions must be assessed based on careful examination of both eyes for other lesions. The veterinarian must methodically examine the eyes for any other lesions suggestive of active or inactive uveitis. For example,
Figure 6. Butterfly type peripapillary scar nasal to the optic disc in a 12-year-old Thoroughbred. The eye was visual, and no other lesions suggestive of uveitis were identified in either eye.
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if either eye has a dark iris, synechiae, pigment that rests on the anterior lens capsule, cataract, vitreal inflammation, or unexplained peripheral corneal vascularization, uveitis should be suspected as the cause of the inactive peripapillary lesion. On the other hand, if both irises are normal and no lesions suggestive of prior ocular inflammation are identified, a unilateral peripapillary scar in a visual eye need not carry a guarded prognosis. Evaluation of the retinal vessels within the lesion also is important because regional disappearance of retinal vessels may indicate a more significant retinal lesion. Obviously, causes other than uveitis may result in peripapillary scars. If this is the only lesion found during a soundness examination, therefore, the buyer should be made aware of the finding and informed of its possible relationship to uveitis but not be informed that the animal is unsound simply because of this lesion. Inform owners or buyers that the horse may have had a prior uveitis episode but, based on the complete ophthalmic examination, there is insufficient evidence to confirm this. In fact, many horses with peripapillary scars or butterfly lesions as their only ophthalmic abnormality (usually unilaterally) never have had uveitis, nor do they develop it. Traumatic Retinal Lesions
Traumatic retinal lesions in horses-including retinal hemorrhages, retinal tears, and retinal detachments-may be associated with skull trauma or blunt ocular injuries from whips, lead shanks, or twitches. Optic nerve lesions also may be present, but discussion of these is deferred to the following section. Blunt injuries causing retinal lesions usually induce anterior segment damage to the cornea and iris. This anterior segment damage (corneal edema from endothelial damage and traumatic iritis) may obscure some fundic details. Small subretinal, intraretinal, or preretinal hemorrhages may eventually resolve with time and not interfere significantly with vision. Large retinal or vitreal hemorrhages, however, generally signal hemorrhage from the uveal tract rather than the retina and carry a guarded prognosis because of the likelihood of chorioretinal scarring and retinal degeneration in affected areas (Figs. 7 and 8). Conservative therapy with systemic nonsteroidal anti-inflammatory medication and topical therapy based on ophthalmic findings are indicated. Assuming no corneal epithelial defects are identified, topical corticosteroids and atropine should be used to control the traumatic anterior uveitis. Retinal and vitreal hemorrhages take weeks or months to resolve and therapy, at best, is supportive rather than curative. Retinal Detachments
Congenital retinal detachments occasionally are the cause of blindness in newborn foals and have been already been discussed under congenital retinal disorders. Acquired retinal detachments in adult
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Figure 7. Retinal hemorrhage following a whip injury to the eye in a 3-year-old Arabian.
horses may be associated with ocular trauma, skull trauma, or equine uveitis, and occur as delayed postsurgical complications of cataract surgery. Occasional idiopathic retinal detachments occur in older horses as well and may be associated with vitreal degenerative processes. Acquired retinal detachments may be partial or complete. Partial retinal detachments cause specific visual field deficits whereas complete detachments cause blindness and loss of direct pupillary light response. Detachments secondary to equine uveitis occur as a sequel to peripapillary vitreoretinal adhesions that cause retinal traction detachments
Figure 8. Same eye as Figure 7 showing subsequent diffuse retinal and optic nerve degeneration 6 months following the acute injury.
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Figure 9. Early-phase vitreoretinal traction band detachments of the retina in the peripapillary region secondary to uveitis in a 6-year-old Standardbred horse.
(Fig. 9). Vitreoretinal traction detachments progress to complete detachment because of vitreal fibrosis. Generally, retinal detachments occur months to years after the initial uveitis and occasionally develop in uveitis-affected eyes that appear to be currently free of anterior segment inflammation. Such detachments may be recognized by a sunburst appearance of multiple radiatory retinal veils attached near the optic disc (Fig. 10). Although
Figure 10. Complete retinal detachment.
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treatment of partial retinal detachment is possible theoretically, on a practical basis, therapy is unlikely to be successful.
OPTIC NERVE Congenital Lesions
Congenital lesions of the optic nerve are extremely rare in horses. Gelatt8 reported one foal with bilateral optic nerve hypoplasia, and Rubin25 refers to a foal with congenital optic nerve atrophy (vascular atrophy and a normal optic disc). If in utero inflammation had been present in these cases, peripapillary lesions suggestive of prior inflammation would be present. Optic nerve hypoplasia may be misdiagnosed in foals with multiple congenital ocular anomalies or luxated lenses, because the optic disc appears smaller ophthalmoscopically because of optical changes in the eye caused by the anomalies. Colobomas of the central optic disc occasionally have been observed in Appaloosas affected with night blindness. These lesions are subtle and are not a characteristic finding in night-blind Appaloosas, given that the fundus typically appears normal in these horses.
Acquired Disorders
Traumatic Damage
Traumatic damage to the optic nerve is associated with skull trauma in horses that fall over backwards or rise up in starting gates, trailers, or stalls with low ceilings. 7, 11, 18 Retrobulbar damage to the optic nerve may occur within the optic canals or at the point of exit from the optic foramen. Although more common as a unilateral lesion, occasional bilateral lesions occur. The result is partial or complete visual loss in the affected eye within 24 hours of injury. Direct pupillary light response is reduced or absent. Ophthalmoscopic lesions, including edema or hemorrhage (Fig. 11), may be present within 24 to 48 hours of the injury, but are not present in many horses because of the retrobulbar nature of the injury. Similar to retrobulbar optic nerve damage in other species, the optic disc may appear normal but the diagnosis is made because "the patient sees nothing and the doctor sees nothing." Edema and hemorrhage in the retrobulbar portion of the affected optic nerve may be most prominent within the bony confines of the optic canals. Because of the nature of horses, severe skull trauma may cause a whiplash-type snapping injury at the cranial aspect of the optic canal, thereby causing extensive physical and inflammatory damage at this point. Ophthalmoscopy immediately postinjury may be difficult in horses that have extensive periorbital trauma, eyelid swelling, or orbital fractures.
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Figure 11. Hemorrhage overlying the optic disc and around one retinal vessel dorsal to the disc in a horse that had suffered skull trauma 24 hours earlier.
Treatment should be intensive and immediate if vision or pupillary light reflexes are reduced. Intravenous dimethylsulfoxide (1 g/kg body weight), systemic nonsteroidal anti-inflammatory drugs, and judicious doses of systemic corticosteroids should be employed and repeated as necessary. As always, the relative value of systemic corticosteroids in this instance must be weighed against their potential dangers (i.e., laminitis, enteritis). Successful therapy should restore pupillary and visual function within 72 hours. Lack of response after this time signals permanent optic nerve damage. Permanent damage eventually leads to an atrophic appearance to the optic disc after several weeks or months due to degeneration of myelinated optic nerve fibers (Fig. 12). Some horses will have partial return of vision with subsequent regional pallor or vascular loss in the optic disc. Infarction
Optic nerve infarction occurs sporadically and may be associated with vascular insults,15 multifocal central nervous system infarction, trauma, or sepsis, or may occur following surgical ligation of carotid artery branches for guttural pouch mycosis. The best opportunity to study ischemic optic nerve lesions has occurred in recent years because of surgical techniques employed for treatment of guttural pouch mycosis. 4 , 5, 6, 10 Ligation or occlusion of the common carotid artery or its branches occasionally results in ipsilateral blindness within 1 week of surgery. A dilated, nonresponsive pupil and complete blindness occur
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Figure 12. Complete optic atrophy subsequent to prior traumatic optic neuropathy in a horse.
in these horses. The author has had the opportunity to follow three such horses in Cornell's teaching hospital. Initial ophthalmoscopic examination finds a very subtle optic disc pallor, although the retinal vessels are still apparent. Within 3 to 5 days, the appearance of the disc changes and perivascular edema typical of venous outflow disturbance are observed. These changes seem to indicate an initial arterial infarction with later venous thrombosis or venous outflow disturbance. Eventual optic atrophy with vascular loss occurs but is not appreciable ophthalmoscopically for weeks following the initial infarction. The prognosis is extremely guarded and, to date, the author has not restored vision in any horse afflicted with this condition, despite symptomatic therapy. If trauma and sepsis are ruled out, the rare idiopathic instances of optic nerve infarction lesions associated with multifocal central nervous system infarction can only be diagnosed absolutely by histopathology following necropsy. Inflammatory Optic Nerve Lesions
Inflammatory optic neuritis in horses most commonly is observed in association with equine uveitis but also may occur rarely in septicemia and multifocal central nervous system infections due to bacterial and protozoan organisms. Optic neuritis in equine uveitis patients may occur alone or in conjunction \vith retinal vasculitis and peripapillary chorioretinitis. 25 These lesions have been observed in uveitis due to leptospirosis,14 Onchocerca cervicalis larvae, 1 and idiopathic immunemediated causes. Papillitis, retinal vasculitis characterized by gray or
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white exudates following the course of retinal vessels, and fluffy peripapillary lesions that appear depigmented may be observed. Short of histopathology, it is difficult to differentiate these lesions from a pure peripapillary chorioretinitis, as previously discussed. One important differentiating sign, however, is the presence or absence of vision. Uveitis patients showing true optic neuritis tend to be blind, while those with only peripapillary chorioretinitis tend to be visual, albeit compromised visually. As in the discussion of retinal inflammation, anterior segment lesions may partially obscure fundic details, thereby further interfering with ophthalmoscopic differentiation of the posterior segment lesions. Septic lesions of the optic nerve have a more malignant course and initially appear as optic disc inflammation characterized by hard or soft exudates, hemorrhage, or edema (Fig. 13). Septic uveitis or endophthalmitis is the feared and usual sequela as the vitreous subsequently is infected. Such lesions have been observed rarely in septicemic foals and adult horses having septicemia, endocarditis,24 or multifocal protozoan encephalomyelitis. Regarding protozoan organisms, both Toxoplasma gondii and Sarcocystis neurona should be considered as possible causative agents, but both rarely cause ophthalmic manifestations in the horse. Bacterial organisms include Streptococcus spp., Actinobacillus equuli, and Rhodococcus equi. Septic lesions usually are observed in fulminating septic situations and carry a grave prognosis for life, in the author's experience. Other causes of optic neuritis are rare. Borna disease, or viral encephalomyelitis, is an exotic viral disease capable of causing optic neuritis in horses but is not seen in the United States. 25 Another inflammatory optic neuritis, termed exudative optic neuritis, has been
Figure 13. Optic nerve septic inflammation, which subsequently progressed to endophthalmitis in a horse having endocarditis.
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recognized in Europe 25 and occasionally in the United States. Hard and soft exudate radiates from the optic disc and is raised into the vitreous, creating a dramatic lesion associated with acute blindness. Hemorrhage also may be evident, radiating from the optic nerve. The cause of this condition is unknown. Sepsis and prior trauma should be ruled out through history, physical examination, and necessary ancillary procedures. Treatment is unlikely to be successful and would be symptomatic, at best. Proliferative Optic Neuropathy
This lesion usually is found as a unilateral incidental finding in aged horses (over 15 years of age). The author has observed the lesion in one horse that was only 6 years of age, however. A pedunculated white mass attached to the periphery of the optic disc protrudes into the vitreous humor (Fig. 14). Much debate exists as to the exact cell origin and components of proliferative optic neuropathy. One report considered the lesions as astrocytoma, 9 whereas another suggested that the foamy cells identified histologically resembled a lipid storage such as observed in human xanthomatosis. 25, 26 The author recently collaborated on a study with histopathologic and electron microscopy of a lesion that suggested a Schwann cell derivation of the granular cells. 21 In any event, the lesions generally are benign and are incidental findings. Larger proliferative optic neuropathic lesions may be observed to wave about in the vitreous when the horse's eye moves. Although generally benign, the lesions do continue to enlarge over months or years. The author has examined two horses over 20 years of
Figure 14. Proliferative optic neuropathy.
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age that had such large proliferative lesions that behavior and vision were affected. The horses became apprehensive on the ipsilateral side. Ophthalmoscopy revealed proliferative optic neuropathies nearly as large as the optic disc itself-large enough to wave noticeably in the vitreous, casting a shadow on the retina ventral to the lesion. Because the lesions generally are benign, no treatment usually is indicated and the author knows of no surgical attempt at removal, to date.
THE VITREOUS Congenital Disorders
Congenital vitreal lesions in the horse are limited to persistent hyaloid arteries and remnants thereof. The hyaloid artery and arterial system (tunica vasculosa lentis) around the lens normally disappear before birth in foals. Persistent hyaloid arteries are less common in newborn foals than in most other domestic neonates but occasionally are observed. A distinct linear structure traversing the vitreous from the optic disc to the axial posterior cortex of the lens will be apparent upon ophthalmoscopy when a hyaloid artery remnant persists. Rarely, this vessel may still contain blood, as it does in the embryonic eye, but usually only a vascular remnant that appears gray-white or dark in color is found. Persistent hyaloid artery remnants found in newborn foals generally disappear by 3 to 4 months of age. The only clinical concern generated by this entity is possible damage to the axial posterior lens capsule and subsequent focal cataract formation at this site. If a cataract is caused at this site, the potential for further cataract formation may exist. Fortunately, these axial capsular cataracts seldom progress and tend to remain stable for the horse's entire life.
Inflammatory Disorders
Vitreal inflammation (vitreitis, vitritis) is extremely common in horses affected with uveitis. Inflammatory cells and fibrin from the inflamed uveal tract may cause diffuse or focal vitreal opacities. Fibrin and porphyrin metabolites that ooze into the vitreous cause a yellowgreen appearance when focal light is directed through the pupil of some horses with uveitis. This color and a generally dull or reduced tapetal reflection signal vitreal inflammation. Clumps, veils, or floating accumulations of vitreal debris may be observed in uveitis-affected eyes and these accumulations generally are mobile when the eye moves. Heavy vitreal accumulations greatly interfere with the horse's vision and obscure fundic details during ophthalmic examination. Severe vitreal inflammation promotes syneresis in the vitreous such that the normal vitreous gel separates into liquid and solid protein (inflamma-
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tory cells and vitreal protein) components. Thus, further mobility is granted the floating debris as the normal vitreous gel liquifies. Vitreal inflammation also may contribute to lenticular metabolic disorders resulting in cataract formation in uveitis patients. Intensive therapies with anti-inflammatory drugs that establish levels in the vitreous are indicated when treating uveitis patients with extensive vitritis. These might include systemic corticosteroids, subconjunctival repository corticosteroid injections, and topical corticosteroids (i.e., prednisolone acetate preparations) that penetrate the cornea sufficiently to establish significant intraocular levels. The prognosis for vitritis is guarded because vitreal degeneration induced by the inflammation is irreversible to some degree. In addition, products (cells, proteins) deposited in the vitreous are "trapped" in this cavity, given the poor resorption capabilities of the posterior segment. Vitreoretinal adhesions also may develop as fibrin strands contract and fibrose, predisposing to retinal detachments. Septic vitritis of embolic origin also is an extremely serious problem since treatment by other than vitrectomy plus intensive systemic, subconjunctival, and topical antibiotic therapy is unlikely to prevent endophthalmitis or panophthalmitis. Septic vitritis is observed occasionally in septicemic foals, and a dense inflammatory cloud is observed in the vitreous. Septic uveitis typically coexists. A grave prognosis is indicated since overwhelming septicemia is the usual cause. The only successful cases managed by the author have been Streptococcal in origin, where systemic and topical chloramphenicol was successful. Most neonatal septicemias are due to gram-negative bacteria (Escherichia coli, Klebsiella, Salmonella, Actinobacillus equuli), however, and vitritis due to these organisms is more difficult to resolve than Streptococcal vitritis.
Vitreal Degeneration
The simplest and most common form of vitreal degeneration is the vitreal floater. Most horses over 6 years of age have some vitreal floaters, as do most adult people. Insignificant or incidental vitreal floaters first appear as refractile mobile strands that can best be observed during ophthalmoscopy and retroillumination using the "0" diopter setting of the direct ophthalmoscope at a distance of 12 to 18 inches (30.5 to 45.7 cm) from the eye. While allowing the horse's eye to move normally, the examiner looks through the ophthalmoscope to highlight these floaters against the colorful tapetal background (Fig. 15). The importance of vitreal floaters is the occasionally real, but usually false, syndrome of the "fly-eyed" horse that appears to shy for no apparent reason. Ruling out extensive vitreal floaters is part of the examination performed on horses with this complaint as well as in horses having the major medical dilemma known as "head shaking." Vitreal floaters seldom are the cause of these conditions, but there are
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Figure 15. Large single vitreal floater highlighted against the colorful tapetal background in an equine eye.
rare instances in which exhaustive medical workups turn up no other reason for the problem. In the author's experience, vitreal floaters causing behavioral changes usually are observed at a rate of one case every 1 or 2 years. More extensive vitreal degeneration in middle-aged or older horses usually is due to vitreal syneresis with fractionation of the vitreous gel into solid and liquid components. This may take several forms, the simplest of which is the development of extensive vitreal strands and floaters that appear dark rather than refractile when viewed against the colorful tapetal background. Most horses with this condition are asymptomatic but, rarely, an animal may show visual or behavioral disturbance. Other types of vitreal degeneration are less common in horses. Asteroid hyalosis or cholesterolosis bulbi appears in horses in a fashion similar to other species. Stationary crystals, thought to be cholesterol or calcium-lipid material, are scattered diffusely through the vitreous like a constellation of stars. The crystals are small (1-2 mm) and refract light during focal light examination of the posterior pole. Asteroid hyalosis in horses usually is an incidental finding that does not appear to affect vision. It is found in older horses that generally are not in performance, so exact statements as to its effects on vision are difficult to interpret. Synchysis scintillans is another degenerative condition of the vitreous occasionally observed in older horses. Vitreal syneresis or liquefaction has occurred in these horses, and the solid component of the vitreous has coalesced into crystalline material that floats and moves freely during normal ocular movements. The appearance has been compared to a snow-scene paperweight in which the particles slowly
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filter through the fluid when the paperweight is moved or inverted. This condition usually is an incidental finding and, similar to asteroid hyalosis, affected horses appear to be visual.
References 1. Cello RM: Ocular onchocerciasis in the horse. Equine Vet J 3:148-154, 1971 2. Crispin SM, Matthews AG, Parker J: The equine fundus, I: Examination, embryology, structure and function. Equine Vet J (suppl)10:42-49, 1990 3. DerKaloustian V, Baghdassarian SA: The autosomal recessive variety of congenital stationary night-blindness with myopia. J Med Genet 9(67):67-69, 1972 4. Freeman DE, Donawick WJ: Occlusion of the internal carotid artery in the horse by means of a balloon-tipped catheter: Evaluation of a method designed to prevent epistaxis caused by guttural pouch mycosis. J Am Vet Med Assoc 176(3):232-235, 1980 5. Freeman DE, Ross MW, Donawick WJ: "Steal phenomenon" proposed as the cause of blindness after arterial occlusion for treatment of guttural pouch mycosis in horses. J Am Vet Med Assoc 197(7):811-812, 1990 6. Freeman DE, Ross MW, Donawick WJ, et al: Occlusion of the external carotid and maxillary arteries in the horse to prevent hemorrhage from guttural pouch mycosis. Vet Surg 18(1):39-47, 1989 7. Gelatt KN: Neuroretinopathy in horses. J Equine Med Surg 3(2):91-96, 1979 8. Gelatt KN, Leipold HW, Coffman JR: Bilateral optic nerve hypoplasia in a colt. J Am Vet Med Assoc 155(4):627-631, 1969 9. Gelatt K, Leipold H, Finocchio E, et al: Optic disc astrocytoma in a horse. Can Vet J 12:53-55, 1971 10. Hardy J, Robertson JT, Wilkie DA: Ischemic optic neuropathy and blindness after arterial occlusion and treatment of guttural pouch mycosis in two horses. J Am Vet Med Assoc 196:1631-1634, 1961 11. Martin L, Kaswan R, Chapman W: Four cases of traumatic optic nerve blindness in the horse. Equine Vet J 18(2):133-137, 1986 12. Matthews AG, Crispin SM, Parker J: The equine fundus, II: Normal anatomical variants and colobomata. Equine Vet J (suppl)10:50-54, 1990 13. Merin S, Rose H, Auerbach E, et al: Syndrome of congenital high myopia with nyctalopia. Am J Ophthalmol 780(4):541-547, 1970 14. Morter RL, Williams RD, Bolte H, et al: Equine leptospirosis. J Am Vet Med Assoc 155:436-442, 1969 15. Platt H, Barnett KC, Barry DR, et al: Degenerative lesions of the optic nerve in Equidae. Equine Vet J (suppl)2:91-97, 1983 16. Rebhun WC: Diagnosis and treatment of equine uveitis. J Am Vet Med Assoc 175(8):803-808, 1979 17. Rebhun WC: Equine retinal lesions and retinal detachments. Equine Vet J (suppl)2:8690, 1983 18. Rebhun WC: Traumatic optic neuropathy: How to prevent permanent blindness. Vet Med Small Anim Clin April:350-353, 1986 19. Rebhun WC, Loew ER, Riis RC: Clinical manifestation of night blindness in the Appaloosa horse. Compend Contin Educ Pract Vet 6(2):S103-5106, 1984 20. Riis RC: Equine ophthalmology. In Gelatt KN (ed): Textbook of Veterinary Ophthalmology. Philadelphia, Lea & Febiger, 1981, pp 569-605 21. Riis RC, Rebhun WC: Proliferative optic neuropathy in a horse caused by a granular cell tumour. Equine Vet J (suppl)10:69-72, 1990 22. Roberts 5J: Sequelae of leptospirosis in horses on a small farm. J Am Vet Med Assoc 133:189-194, 1958 23. Roberts SR: Chorioretinitis in a band of horses. J Am Vet Med Assoc 158(12):20432046, 1971
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24. Ross CE, Rebhun WC, Dietze AE, et al: Case report: Endocarditis and optic neuritis in a Quarter Horse mare. Compend Contin Educ Pract Vet 9(4):451-454, 1987 25. Rubin LF: Atlas of Veterinary Ophthalmoscopy. Philadelphia, Lea & Febiger, 1974 26. Saunders LZ, Bistner 51, Rubin LF: Proliferative optic neuropathy in horses. Vet Pathol 9:368-378, 1972 27. Syversen D: Sex-linked essential nyctalopia in a Norwegian family. Acta Ophthalmol 52(1):145-149, 1974 28. Volker-Dieben HJ, Went LN: Ophthalmologic and genetic study of a family with nyctalopia and myopia. Ophthalmologica 171:358-359, 1975 29. Witzel DA, Joyce JR, Smith EL: Electroretinography of congenital night blindness in the Appaloosa filly. J Equine Med Surg 1(6):226-229, 1977 30. Witzel DA, Riis RC, Rebhun WC, et al: Night blindness in the Appaloosa: A sibling occurrence. J Equine Med Surg 1(11):383-386, 1977
Address reprint requests to William C. Rebhun, DVM Department of Clinical Sciences Cornell University College of Veterinary Medicine Ithaca, NY 14853
