Decreased Vision in Dogs and Cats

Recognizing gradual vision loss, its causes, and what can be done

Written by Siniša D. Grozdanić, DVM, PhD, Diplomate ACVO, veterinary ophthalmologist, Animal Eye Consultants of Iowa. Medically reviewed: October 2026.

The short answer

Vision can decline slowly over weeks to years, and pets adapt so well that owners often notice only when the loss is advanced. Common causes include cataracts, inherited retinal diseases such as progressive retinal atrophy (PRA), chronic glaucoma, corneal scarring or pigment, immune-mediated retinal disease, high blood pressure, and certain medications.^[1,2]

Many causes are treatable, and others can be slowed or managed. Even SARDS, an autoimmune retinal disease, often has an early stage that is easy to miss but can respond well to treatment.^[22,23] Genetic testing can prevent inherited blindness in future generations. If your pet seems to see poorly, especially at night or in unfamiliar places, schedule an eye examination.

Signs of decreased vision

• Hesitation or bumping into objects in dim light or at night (night blindness is often the first sign of retinal disease)
• Reluctance to go outside after dark, use stairs, or jump on or off furniture
• Difficulty in bright light or sunlight. This day blindness is typical of inherited cone diseases.
• Missing tossed treats or toys, or difficulty finding a food bowl or water
• Poor depth perception: misjudging steps, curbs, and jumps (cats often miss jumps)
• Walking slowly with the nose to the ground, following walls, or staying close to the owner
• Startling when approached, or new anxiety or clinginess
• Wide pupils, more noticeable “eye shine,” or cloudy-looking eyes
• Vision problems that seem worse in new surroundings, such as on vacation or after moving furniture

Because gradual vision loss is so well hidden, owners frequently describe it as “sudden” when it is first noticed in an unfamiliar environment.^[1]

How vision works and where it can fail

For a pet to see, light must pass through a clear cornea, aqueous fluid, lens, and vitreous to reach the retina. There, rods provide vision in dim light and cones provide vision in daylight and color vision. The retina converts light into electrical signals that travel through the optic nerve to the brain. Dogs and cats have many more rods than people, and a reflective tapetum behind the retina, which gives them excellent night vision. This is also why rod diseases such as PRA first cause night blindness.^[1,2]

Normal canine fundus: the optic nerve head, retinal blood vessels, and reflective tapetum.

How we test vision

Pets can’t read an eye chart, so we combine several objective tests:^[1,3]

• Behavioral vision testing: menace and dazzle responses, following a cotton ball or toy, and navigating an obstacle course in bright and dim light
• Chromatic pupil light reflex (cPLR) testing: developed by Dr. Grozdanić and colleagues. Red light tests the outer retina (rods and cones), and blue light tests special light-sensitive cells of the inner retina and optic nerve. A poor red / good blue response points to outer retinal disease, while no red / no blue points to optic nerve or brain disease. It is the most sensitive screening test for early SARDS, and it should be performed before any bright examination light is used.^[3,22,24]
• Electroretinography (ERG): measures the electrical response of the rods and cones. It can detect inherited retinal disease and drug toxicity before any changes are visible, and it is required before cataract surgery.
• Optical coherence tomography (OCT): cross-sectional, microscopic-resolution imaging of the retinal layers^[12]
• Fundus examination and photography: to look for thinning, scarring, bleeding, detachment, or optic nerve changes
• Genetic testing: DNA tests are available for many inherited eye diseases^[4,5]

Obstacle-course (visual maze) testing in bright and dim light helps detect day and night vision deficits.

Depth perception and distance vision testing in an open arena.

Chromatic pupil light reflex in outer retinal disease: a poor response to red light (A) with a good response to blue light (B).

Chromatic pupil light reflex in optic nerve disease: no response to red (A) or blue (B) light.

Vision loss from the front of the eye

Cataracts

Cataracts are the most common treatable cause of decreased vision. About half of dogs have some lens opacity by around 9.4 years of age, and every dog older than 13.5 years in one large study had some lens change.^[17] Inherited cataracts can develop in young dogs, and diabetic cataracts can mature within weeks. Cataract surgery restores functional vision in most dogs when the retina is healthy. In one study, 83% of eyes were visual at the final recheck.^[18] Because cataracts can hide retinal disease such as PRA, we perform an ERG and ocular ultrasound before surgery. Normal age-related lens haze (nuclear sclerosis) looks similar to owners but does not cause blindness. See our Cloudy Eye and Cataracts pages.

Mature diabetic cataract with inflammation of the surrounding eye tissue.

Corneal opacities

Chronic corneal diseases block light gradually. They include pannus in German Shepherds and Greyhounds, pigmentary keratitis in Pugs and other flat-faced breeds (82% of 295 Pugs in one study had some corneal pigment), corneal dystrophies, and endothelial degeneration in older dogs. Most can be controlled with long-term eye drops or surgery, especially when treated early.^[1,20] See our Corneal Disease page.

Pannus (chronic superficial keratitis): pink vascular tissue and pigment growing across the cornea.

Pigmentary keratitis in a brachycephalic dog: brown pigment spreading across the cornea.

Chronic glaucoma

Glaucoma is a leading cause of permanent blindness in dogs. Some forms, such as the slowly progressive inherited glaucoma of Beagles and some other breeds, steal vision gradually with few outward signs, until the optic nerve is severely damaged. Regular eye-pressure checks are recommended for predisposed breeds and for the second eye of any dog that has had glaucoma.^[19]

Glaucoma: congested episcleral vessels, a dilated pupil, and a hazy cornea.

Inherited retinal diseases

Dogs have more naturally occurring inherited retinal diseases than any other species except humans. Many are caused by the same genes that cause retinitis pigmentosa, Stargardt disease, Best disease, Leber congenital amaurosis, and achromatopsia in people. This makes dogs important “large animal models” for developing treatments for both species.^[4,7]

Progressive retinal atrophy (PRA)

PRA is a group of inherited diseases in which the rods, and later the cones, degenerate. It affects around 100 dog breeds and several cat breeds. Typically, night vision fails first, followed by day vision, over months to years. The pupils become dilated and the eyes look shinier. Cataracts often develop late in the disease. PRA is not painful, and affected pets adapt remarkably well.^[1,4] See our progressive retinal atrophy page.

Examples of PRA genes and breeds include:^[4]

PRA is genetically diverse. In a study of 21 breeds with known PRA mutations, most breeds also had affected dogs that carried none of the known mutations. A negative DNA test therefore does not completely rule out PRA, and an eye examination with ERG remains important.^[5]

Progressive retinal atrophy: attenuated retinal vessels and tapetal hyperreflectivity from retinal thinning.

Day blindness, cone and cone-rod diseases

Achromatopsia (cone degeneration) causes day blindness and lack of color vision, while night vision is preserved. It is caused by CNGB3 mutations in Alaskan Malamutes and German Shorthaired Pointers, and by CNGA3 mutations in German Shepherds.^[8] Cone-rod dystrophies, including an ABCA4-related form in Labrador Retrievers and a form in Miniature Wire-haired Dachshunds, primarily affect daylight vision first.^[4]

Canine multifocal retinopathy (CMR)

CMR is caused by mutations in the BEST1 gene, the same gene that causes Best disease in people. It produces multiple raised, blister-like areas of retinal detachment, starting in young puppies. It affects Great Pyrenees, Mastiffs and related breeds (cmr1), Coton de Tulear (cmr2), and Lapponian Herders (cmr3). It is often only mildly progressive, but bright light can trigger new micro-detachments.^[9]

Congenital diseases

Collie eye anomaly (CEA), caused by a deletion in the NHEJ1 gene, affects Collies, Shetland Sheepdogs, Australian Shepherds, Border Collies, and related breeds. Most dogs see reasonably well, but those with large colobomas risk retinal detachment and bleeding.^[10] Retinal dysplasia, optic nerve hypoplasia, and congenital stationary night blindness (an RPE65-related disease in Briards; also seen in Appaloosa horses with leopard-spotting coat patterns) are other congenital causes of reduced vision.^[1,4]

Collie eye anomaly with choroidal hypoplasia and abnormal choroidal vessels.

Gene therapy: from dogs to people

In 2001, gene therapy restored vision in Briard dogs with RPE65 retinal disease. This landmark study paved the way for human clinical trials in Leber congenital amaurosis.^[6,7] Since then, experimental gene therapies have shown success in dogs with CNGB1 PRA, rhodopsin-related PRA, achromatopsia (CNGA3 and CNGB3), X-linked PRA, and BEST1-related multifocal retinopathy.^[7] These treatments are still at the research stage and are not yet available as routine clinical treatment for pets. Genetic testing and responsible breeding remain the most effective ways to prevent inherited blindness.

Genetic testing and breeding

Annual eye examinations by a board-certified veterinary ophthalmologist (for example, OFA Companion Animal Eye Registry exams) and breed-appropriate DNA tests help breeders avoid producing affected puppies. Carriers of recessive diseases can still be bred responsibly to tested, clear mates. Dogs affected by PRA, Collie eye anomaly with colobomas, or other inherited blinding diseases should not be bred.^[4,5,10]

Acquired retinal diseases

SARDS and immune-mediated retinitis (IMR): often not so “sudden”

Sudden acquired retinal degeneration syndrome (SARDS) and immune-mediated retinitis (IMR) are autoimmune retinal diseases, and a major focus of Dr. Grozdanić’s research.^[11,12,21] SARDS is classically described as blindness that develops over days to weeks. Our studies show that many dogs have a detectable early phase while they can still see well in daylight. In that phase, vision can often be preserved with treatment.^[22,23] Based on this work, Dr. Grozdanić proposed describing the disease in three stages: early, intermediate, and advanced SARDS.^[23]

Warning signs that suggest early SARDS or IMR

• Sudden onset of night blindness, or vision problems that come and go (day or night)
• Pupils that look larger than usual
• Reluctance to use stairs or jump on and off the bed, especially in dim light; trouble finding small objects up close or seeing distant objects
• A history of allergies (seasonal, food, vaccine, or drug reactions) or other autoimmune disease
• Increased thirst, urination, or appetite; unexplained weight gain; decreased activity; or intermittent lethargy or neurological episodes
• Laboratory changes such as elevated liver enzymes (ALP, ALT), high cholesterol or lipids, protein in the urine, dilute urine, high blood pressure, or endocrine disease (hypothyroidism, Cushing’s disease, pancreatitis)

What our research has shown

Early SARDS and IMR (57 dogs with normal or near-normal day vision, presented at the 2013 American College of Veterinary Ophthalmologists meeting):^[22]

• 98% (54 of 55 tested dogs) had an abnormal pupil response to red light, the key screening finding.
• 82% of dogs tested with flicker ERG had an abnormal response, while 47% still had a normal standard (full-field) ERG.
• 42% had night blindness, usually of sudden onset; 82% had a history of autoimmune disease; and 88% had a pale-appearing optic nerve head.
• Without immunosuppressive treatment, 47% of dogs declined or became completely blind (follow-up 15 to 96 months).
• With immunosuppressive treatment, 97% (38 of 39) kept stable or improved vision for 12 to 72 months.

The fundus in early SARDS often looks normal (A). The most frequent finding is a pale optic nerve head with thin blood vessels (B). Subtle hyperreflective changes along the vessels (C) are also common.

Electroretinography in early SARDS: a standard scotopic ERG can still be normal (A) while the 20 Hz flicker response is absent (B). This is why flicker testing is important for early diagnosis.

Intermediate SARDS (21 dogs with normal day vision but a completely flat ERG, presented at the 2016 American College of Veterinary Ophthalmologists meeting):^[23]

• Median age was 9 years, and vision problems had been noticed for a median of 3 months. 81% had a history of autoimmune disease, and 75% had increased thirst, urination, or appetite, many with elevated liver enzymes.
• All 7 dogs that received no treatment, a single immunosuppressive drug, or stopped therapy lost vision within 1 to 9 months.
• Of 14 dogs treated with a combination of two or three immunomodulating medications, 13 kept their vision for up to 24 months of follow-up. In this group, the risk of blindness was about 50 times lower than with no treatment or single-drug treatment.

Intermediate SARDS: proportion of dogs that remained visual over time with combination therapy (green) versus no therapy or single-drug therapy (red). Hazard ratio about 50; p = 0.0006.

Other observations. In our patients, stopping immunosuppressive treatment was sometimes followed by blindness within weeks to months, and some dogs appeared to worsen after general anesthesia. These are individual case observations, but they are why we recommend that treatment changes and elective anesthesia be discussed with your ophthalmologist. Most dogs with early SARDS were receiving ivermectin-based heartworm prevention at diagnosis. Because these products are so widely used, the meaning of this finding is still being studied (see the next section).^[22,23]

What this means for your pet: the earlier SARDS is detected, the better the chance of saving vision. The approach depends on stage: a single medication is often effective in early disease, while intermediate disease generally needs a combination of medications. Results in completely blind dogs are much less predictable. Treatment is long-term and requires regular monitoring of vision, ERG, and blood work.^[22,23] See our SARDS & IMR page.

Advanced SARDS: a pale optic nerve head (A) and an extinguished (“flat”) electroretinogram (B).

Range of fundus changes in dogs with SARDS and IMR (A–F).

Medication-related retinal toxicity

Anti-parasitic medications. In research presented at the 2018 American College of Veterinary Ophthalmologists meeting, Dr. Grozdanić and colleagues described retinal changes in dogs receiving parasite-prevention drugs that act on GABA receptors. These included ivermectin-based heartworm preventives and, in some dogs, oral isoxazoline flea and tick products.^[13] Findings included:

• In kennels using an off-label, concentrated ivermectin dose (about 200 µg/kg monthly, far above the standard heartworm-prevention dose), 43 of 83 dogs (52%) had retinal lesions.
• In screening of 487 dogs from 27 U.S. hospitals receiving routine monthly ivermectin heartworm prevention, 21% had abnormal chromatic pupil responses, compared with 1 of 108 age-matched dogs (0.9%) in the Czech Republic that had never received heartworm prevention.
• In dogs referred for suspected toxicity, signs included night blindness, poor depth perception, difficulty detecting near or far objects, abnormal cPLR responses, retinal lesions, and reduced ERG responses.

Perivascular retinal lesions (arrows), with chorioretinal scars and hyperreflective spots along the blood vessels, in dogs exposed to high-dose ivermectin.

Retinal lesions after high-dose ivermectin exposure that resemble retinal dysplasia (arrows). This could complicate breeding-related eye certification.

Fundus changes in a dog receiving combined ivermectin and oral isoxazoline parasite prevention.

MDR1 gene mutation. Collies, Australian Shepherds, Shetland Sheepdogs, and related herding breeds can carry a mutation in the MDR1 gene, which allows certain drugs such as ivermectin to build up in the brain and retina. At high doses this causes neurological signs and blindness. A DNA test is available.^[14]

Collies and related herding breeds are at increased risk of ivermectin toxicity because of the MDR1 gene mutation.

Fluoroquinolone antibiotics in cats. Enrofloxacin, especially at higher doses or in cats with kidney or liver disease, can cause retinal degeneration and permanent blindness.^[15]

Retinal degeneration after fluoroquinolone treatment in a cat: diffuse tapetal hyperreflectivity and thin retinal vessels.

High blood pressure, infections, and nutrition

High blood pressure, most often linked to kidney disease or hyperthyroidism in cats, causes retinal swelling, bleeding, and detachment. It can reduce vision gradually before causing sudden blindness, so blood pressure should be checked in every older cat with vision problems.^[16] See our hypertensive retinopathy page. Fungal, tick-borne, and protozoal infections can cause chorioretinitis and scarring. In cats, taurine deficiency from inappropriate home-made or poorly formulated diets causes central retinal degeneration, so cats should be fed complete, balanced diets.^[1,2]

Hypertensive retinopathy in a cat: multiple dull areas where fluid has collected under the retina.

Choroidal granuloma caused by systemic blastomycosis.

Optic nerve and brain causes

Optic nerve damage from glaucoma, inflammation (optic neuritis), compression, or underdevelopment (optic nerve hypoplasia) reduces vision, often with a no red / no blue pupil response. Brain tumors, inflammation, and hydrocephalus can cause gradual vision loss with normal-looking eyes, usually along with behavioral or neurological changes. These cases are investigated with MRI or CT.^[1,2,3]

Optic neuritis: a swollen optic nerve head with engorged retinal veins.

MRI of a dog’s brain with a lesion (arrow) affecting the visual pathways.

Living with reduced vision

• Keep furniture, food, and water bowls in the same places, and block stairs and pools.
• Use night lights at home and a leash outdoors after dark.
• Use verbal cues, scent markers, and textured rugs to help your pet navigate.
• Approach and touch your pet gently while speaking, to avoid startling it.
• Continue play using toys that make noise or have a scent.
• Schedule regular rechecks. Cataracts, glaucoma, and inflammation can develop in eyes with retinal disease and may need treatment for comfort.

Most dogs and cats with reduced or no vision adapt very well and enjoy an excellent quality of life.

For referring veterinarians

Practical approach to the patient with decreased vision

1. Document the history: night versus day vision deficits, onset, progression, medications (including parasite preventives and fluoroquinolones), diet, and systemic signs.
2. Screen with dazzle, menace, and maze testing in bright and dim light, and with chromatic PLR. Poor red / good blue = outer retina; no red / no blue = optic nerve or CNS.^[3]
3. Early SARDS/IMR suspects (poor red / good blue cPLR with a normal or near-normal fundus): perform menace and cotton-ball tracking in bright and dim light; check blood pressure, CBC, chemistry, and urinalysis with microalbumin, T4/TSH, and an adrenal panel; and freeze a serum sample for research biomarker testing. Then refer for flicker ERG. Early disease often responds to a single immunomodulating drug, but intermediate SARDS (normal day vision with a flat ERG) generally needs combination therapy, and single-drug therapy failed in all such dogs in our series.^[22,23]
4. Measure blood pressure in all cats, and check IOP in all dogs. Remember that early chronic glaucoma may have few outward signs.^[16,19]
5. Refer for ERG and OCT when the fundus looks normal but vision or cPLR is abnormal (early PRA, SARDS/IMR, drug-related toxicity, cone disease), and before cataract surgery.^[11,12]
6. Recommend breed-appropriate DNA testing and annual eye certification exams for breeding animals. A negative PRA DNA test does not exclude PRA.^[5]
7. Consider annual vision and retinal screening for dogs on long-term GABA-ergic anti-parasitic medications, particularly those with pre-existing retinal or inflammatory eye disease. Avoid off-label concentrated ivermectin.^[13]

Dr. Grozdanić offers free case consultation for veterinarians.

Frequently asked questions

Concerned about your pet's vision?

Contact Animal Eye Consultants of Iowa for a complete vision evaluation, including chromatic pupil light reflex testing, electroretinography, and OCT, by a board-certified veterinary ophthalmologist at our Hiawatha / Cedar Rapids or Quad Cities / Bettendorf location.

Related topics in our Health Library

This information is for educational purposes and does not replace an examination. Every eye condition requires an individual diagnosis and treatment plan.

Scientific references