The retina is one of the most metabolically active tissues in the body. It consists of 10 layers of cells and nerve fibers. Nine layers compose the sensory retina, with a final layer, the retinal pigment epithelium (RPE), present next to the choroids (the primary blood supply to the horse retina). Light passing through the cornea, anterior chamber, lens, and vitreous is absorbed and organized by retinal cells, which then transform the light into electrical signals that pass along the optic nerve fibers to the brain. A reflective tissue called the tapetum in the upper choroid improves night vision. The retina, retinal blood vessels, tapetum, and optic disc (the front of the optic nerve) can be seen with special instruments called ophthalmoscopes (see Figure 1 on page 40 and photo on page 42). Diseases of the retina and optic nerve are respectively termed retinopathies and optic neuropathies.


Chorioretinitis is inflammation of the choroid and retina. It can be caused by infectious agents such as leptospirosis, equine herpesvirus-1, Onchocerca cervicalis, a poorly controlled immune system, trauma, or vascular (blood vessel) disease. Chorioretinitis can be found with or without the signs of anterior uveitis present with equine recurrent uveitis (ERU). The tapetal region is rarely affected in horses. Chorioretinitis can be seen in equine eyes as focal "bullet-hole" retinal lesions, diffuse (spread out) retinal lesions, horizontal bands in the non-tapetum (non-reflective part of the back of the eye) and chorioretinal degeneration near the optic nerve head (see Figure 4 on page 40). Inactive chorioretinitis lesions are more often reported than active lesions, however the reason for this is not known.

Active chorioretinitis appears as focal white spots with indistinct edges, and as large, diffuse gelatinous gray regions of retinal edema (fluid swelling). Inactive chorioretinitis can appear as circular depigmented white regions with hyperpigmented (darkened) centers, or large areas of depigmentation that appear in some cases similar to the wings of a butterfly. Systemic non-steroidal anti-inflammatory drugs (NSAIDs) like flunixin meglumine (Banamine) or phenylbutazone (Bute) are indicated for chorioretinitis to help control the inflammation. Topical medication does not reach the retina and is only indicated if signs of anterior uveitis are also present.

Congenital Stationary Night Blindness

Congenital stationary night blindness (CSNB) is found mainly in the Appaloosa, and it is inherited as a recessive trait. Cases are also noted in Thoroughbreds, Paso Finos, and Standardbreds. CSNB appears to be caused by a failure of neurotransmission in the middle retina. Clinical signs include visual impairment in the dark with generally normal vision in daylight. There is behavioral uneasiness and unpredictability at night. CSNB does not generally progress, hence its name, but horses with progression to vision difficulties in the daytime have been noted. An ophthalmoscopic examination of horses with CSNB will look normal to the veterinarian's eyes. Diagnosis is by clinical signs, breed type, and electroretinogram (ERG). The ERG is a test of retinal function commonly performed by veterinary ophthalmologists. There is no therapy for this condition, but affected animals should not be bred because the condition is heritable. Keeping horses stalled at night with a light on and avoiding exercise in the dark can help the horse feel more comfortable.

Retinal Detachment

Retinal detachment is a separation of the nine layers of the sensory retina from the retinal pigment epithelium. It is associated with slowly progressive, or acute, blindness in horses. It can be congenital in newborn foals or acquired later in life in adults. Retinal detachment can occur in both eyes or in one eye, and detachment can be partial or complete. Retinal detachments are a complication of equine recurrent uveitis (ERU), and they are also associated with congenitally small eyes in foals, head trauma, wounds to the eye that cause the cornea to rupture, cataract surgery, or they can be secondary to intraocular tumors (those within the eye).

Complete retinal detachments are seen as free-floating, moving gray veils in the vitreous overlying the optic disc. The tapetum is brighter than normal. If there is corneal edema, a cataract, or a cloudy vitreous present, the retina might be visible. Ultrasound equipment can be used to diagnose the classic bird-like "seagull sign" of retinal detachment. There is no therapy available in horses. Laser surgery reattachment of the retina is well described for the dog, but has not yet been reported for the horse.

Optic Nerve Disease

Optic nerve hypoplasia--The long nerve fibers of a single retinal cell--the retinal ganglion cell--form the optic nerve. Congenital lack of retinal ganglion cell development, or excessive destruction of ganglion cells in the horse embryo, results in optic nerve hypoplasia (small optic nerve). It can be in one eye or both eyes. Optic nerve hypoplasia might be associated with congenitally small eyes, cataracts, and abnormal retinal development (dysplasia). The optic discs are small and pale with fewer than normal retinal blood vessels present, and there is a large posterior depression of the optic disc. Depending on the degree of optic nerve hypoplasia, the eye might have some vision or be completely blind. A dilated pupil with slow to absent pupillary light reflex (PLR) is present. There is no therapy for this non-progressive condition.

Optic nerve atrophy--The optic nerve shrinks following various types of disease. Atrophy of the optic nerve can be due to inflammatory or non-inflammatory causes. In the early stages of disease, the appearance of the optic nerve disc via ophthalmoscope might be normal although the eye is blind. With time, the optic disc becomes pale with a profound reduction in retinal blood vessels, and an obvious rough appearance or granularity of the optic disc due to loss of the insulation material that normally surrounds each optic nerve fiber (see Figure 2 at left) occurs. Blindness and pupil dilation are the main clinical signs.

Causes and risk factors include optic neuritis (inflammation of the optic nerve), ERU, chorioretinitis, trauma, glaucoma, toxins, neoplasia, and blood loss. Differential diagnosis (signs that distinguish this from other problems) includes optic nerve hypoplasia, retinal detachment, glaucoma, and cataract. There is no therapy for this condition.

Optic neuritis--This inflammation of the optic nerve results in sudden blindness and can occur in both eyes. Exudative (fluid-filled) optic neuritis is a condition of both optic nerves found in older horses. The optic discs in exudative optic neuritis are swollen with large, whitish, raised nodular masses spread across the surface of the optic disc. Retinal and optic disc hemorrhages might be present. The etiology is unknown. There's no known therapy, although corticosteroids and NSAIDs can be given systemically to reduce pain and inflammation. There is a poor prognosis for vision.

Proliferative optic neuropathy (PON)--This optic nerve condition is found primarily in horses older than 15 years. It is usually in one eye with no signs of pain. There is little to no effect on vision in most cases. A slowly enlarging white mass protruding from the optic disc into the vitreous can be seen with the ophthalmoscope (see Figure 4). The lesion might "wiggle" when the eye moves. PON is a proliferation of peripheral nerve cells and resembles a benign tumor (see Figure 3). No therapy is necessary for this condition.

Ischemic optic neuropathy--Head trauma, optic neuritis, severe systemic blood loss, infectious blockage of large blood vessels, and surgical ligation (tying-off) of large blood vessels to the head to prevent severe nose bleeds caused by guttural pouch fungal infection can cause severe lack of oxygen (ischemia) to the optic nerve and retina. This can result in sudden, irreversible blindness in horses. Following a sudden loss of blood supply, the optic disc at first appears slightly pale. Within three to five days, white, raised lesions of the retina appear overlying the optic nerve and its margins. After several weeks there are ophthalmoscopic signs of retinal and optic nerve atrophy. Treatment is symptomatic depending on the cause and if specific infectious agents have been identified. There is a very poor prognosis for return of vision.

Traumatic optic neuropathy--Sudden blindness as a result of a horse falling over backward and traumatizing the top of his skull can occur. This traumatic optic neuropathy results from tearing of the connective tissue covering the optic nerve, or direct compression of the optic nerve associated with hemorrhage or fracture of the skull. In early stages, the optic disc might either appear normal, or be red and swollen. There can be extrusion of optic disc material into the vitreous, and rapid development of optic nerve atrophy is noted. If both eyes are affected, both pupils are dilated with no signs of eye pain. Immediate and aggressive systemic non-steroidal and/or steroidal anti-inflammatory therapy can help preserve vision in some cases.

Sudden Blindness

Acute, sudden blindness might be associated with head or eye trauma, ERU, glaucoma, cataracts, intraocular hemorrhage, optic neuritis, retinal detachment, or brain disease. Newly blind horses are extremely agitated, anxious, and can be dangerous. Horses recovering from anesthesia following removal of sighted eyes because of tumors or infection can be very confused and agitated in the postoperative period. Extreme care should be utilized and the animals approached cautiously on the newly blinded surgical side until the horse adapts to his condition. Horses can adapt amazingly well to blindness, whether in one eye or both eyes, if allowed time to adjust. Several web sites are devoted to the care of blind animals. Simply type "blind horses" into an Internet search engine.

Editor's note: This is the twelfth in a series of eye articles by Dr. Brooks. See the first article, "Eye Anatomy and Physiology," article #2797 at, for more information on normal eye anatomy.

About the Author

Dennis E. Brooks, DVM, PhD, Dipl. ACVO

Dennis E. Brooks, DVM, PhD, Dipl. ACVO, is a professor of ophthalmology at the University of Florida. He has lectured extensively, nationally and internationally, in comparative ophthalmology and glaucoma, and has more than 140 refereed publications. He is a recognized authority on canine glaucoma, and infectious keratitis, corneal transplantation, and glaucoma of horses.

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