The initial retinal degenerative symptoms of retinitis pigmentosa are characterized by decreased night vision (nyctalopia) and the loss of the mid-peripheral visual field. The rod photoreceptor cells, which are responsible for low-light vision and are orientated in the retinal periphery, are the retinal processes affected first during non-syndromic forms of this disease. Visual decline progresses relatively quickly to the far peripheral field, eventually extending into the central visual field as tunnel vision increases. Visual acuity and color vision can become compromised due to accompanying abnormalities in the cone photoreceptor cells, which are responsible for color vision, visual acuity, and sight in the central visual field. The progression of disease symptoms occurs in a symmetrical manner, with both the left and right eyes experiencing symptoms at a similar rate.

A variety of indirect symptoms characterize retinitis pigmentosa along with the direct effects of the initial rod photoreceptor degeneration and later cone photoreceptor decline. Phenomena such as photophobia, which describes the event in which light is perceived as an intense glare, and photopsia, the presence of blinking or shimmering lights within the visual field, often manifest during the later stages of RP. Findings related to RP have often been characterized in the fundus of the eye as the "ophthalamic triad". This includes the development of (1) a mottled appearance of the retinal pigment epithelium (RPE) caused by bone spicule formation, (2) a waxy appearance of the optic nerve, and (3) the attentuation of blood vessels in the retina.

Non-syndromic RP usually presents a variety of the following symptoms:

- Night blindness

- Tunnel vision (due to loss of peripheral vision)

- Latticework vision

- Photopsia (blinking/shimmering lights)

- Photophobia (aversion to glare)

- Development of bone spicules in the fundus

- Slow adjustment from dark to light environments and vice versa

- Blurring of vision

- Poor color separation

- Loss of central vision

- Eventual blindness

There is another retinal disease in Briards known as hereditary retinal dysplasia. These dogs are night blind from birth, and day vision varies. Puppies affected often have nystagmus. It is also known as lipid retinopathy.

Congenital cataracts refers to a lens opacity present at birth. Congenital cataracts cover a broad spectrum of severity: whereas some lens opacities do not progress and are visually insignificant, others can produce profound visual impairment.

Congenital cataracts may be unilateral or bilateral. They can be classified by morphology, presumed or defined genetic cause, presence of specific metabolic disorders, or associated ocular anomalies or systemic findings.

Congenital cataracts occur in a variety of morphologic configurations, including lamellar, polar, sutural, coronary, cerulean, nuclear, capsular, complete, membranous.

Vitelliform macular dystrophy or vitelliform dystrophy is an irregular autosomal dominant eye disorder which can cause progressive vision loss. This disorder affects the retina, specifically cells in a small area near the center of the retina called the macula. The macula is responsible for sharp central vision, which is needed for detailed tasks such as reading, driving, and recognizing faces. The condition is characterized by yellow (or orange), slightly elevated, round structures similar to the yolk (Latin "vitellus") of an egg.

Patients with idiopathic macular telangiectasia type 1 are typically 40 years of age or older. They may have a coincident history of ischemic vascular diseases such as diabetes or hypertension, but these do not appear to be causative factors.

Macular telangiectasia type 2 usually present first between the ages of 50 and 60 years, with a mean age of 55–59 years. They may present with a wide range of visual impact, from totally asymptomatic to substantially impaired; in most cases however, patients retain functional acuity of 20/200 or better. Metamorphopsia may be a subjective complaint. Due to the development of paracentral scotomota (blind spots), reading ability is impaired early in the disease course. It might be even the first symptom of the disease.

The condition may remain stable for extended periods, sometimes interspersed with sudden decreases in vision. Patients’ loss of visual function is disproportionately worse than the impairment of their visual acuity, which is only mildly affected in many cases. In patients with MacTel, as compared with a reference population, there is a significantly higher prevalence of systemic conditions associated with vascular disease, including history of hypertension, history of diabetes, and history of coronary disease. MacTel does not cause total blindness, yet it commonly causes gradual loss of the central vision required for reading and driving.

The most common sign of CEA is the presence of an area of undeveloped choroid (appearing as a pale spot) lateral to the optic disc. The choroid is a collection of blood vessels supplying the retina. CEA can also cause retinal or scleral coloboma, coloboma of the optic disc, retinal detachment, or intraocular hemorrhage. It can be diagnosed by fundoscopy by the age of six or seven weeks. Severe cases may be blind.

Collie eye anomaly (CEA) is a congenital, inherited, bilateral eye disease of dogs, which affects the retina, choroid, and sclera. It can be a mild disease or cause blindness. CEA is caused by a simple autosomal recessive gene defect. There is no treatment.

In general, PRAs are characterised by initial loss of rod photoreceptor cell function followed by that of the cones and for this reason night blindness is the first significant clinical sign for most dogs affected with PRA. As other retinal disorders, PRA can be divided into either dysplastic disease, where the cells develop abnormally, and degenerative, where the cells develop normally but then degenerate during the dog's lifetime.

Generalized PRA is the most common type and causes atrophy of all the neural retinal structures. Central progressive retinal atrophy (CPRA) is a different disease from PRA involving the retinal pigment epithelium (RPE), and is also known as retinal pigment epithelial dystrophy (RPED).

RP may be:

(1) Non-syndromic, that is, it occurs alone, without any other clinical findings,

(2) Syndromic, with other neurosensory disorders, developmental abnormalities, or complex clinical findings, or

(3) Secondary to other systemic diseases.

- RP combined with deafness (congenital or progressive) is called Usher syndrome.

- Alport's syndrome is associated with RP and an abnormal glomerular-basement membrane leading nephrotic syndrome and inherited as X-linked dominant.

- RP combined with ophthalmoplegia, dysphagia, ataxia, and cardiac conduction defects is seen in the mitochondrial DNA disorder Kearns-Sayre syndrome (also known as Ragged Red Fiber Myopathy)

- RP combined with retardation, peripheral neuropathy, acanthotic (spiked) RBCs, ataxia, steatorrhea, is absence of VLDL is seen in abetalipoproteinemia.

- RP is seen clinically in association with several other rare genetic disorders (including muscular dystrophy and chronic granulomatous disease) as part of McLeod syndrome. This is an X-linked recessive phenotype characterized by a complete absence of XK cell surface proteins, and therefore markedly reduced expression of all Kell red blood cell antigens. For transfusion purposes these patients are considered completely incompatible with all normal and K0/K0 donors.

- RP associated with hypogonadism, and developmental delay with an autosomal recessive inheritance pattern is seen with Bardet-Biedl syndrome

Other conditions include neurosyphilis, toxoplasmosis and Refsum's disease.

Signs and symptoms of macular degeneration include:

- Visual symptoms

- Distorted vision in the form of metamorphopsia, in which a grid of straight lines appears wavy and parts of the grid may appear blank: Patients often first notice this when looking at things like miniblinds in their home or telephone poles while driving. There may also be central scotomas, shadows or missing areas of vision

- Slow recovery of visual function after exposure to bright light (photostress test)

- Visual acuity drastically decreasing (two levels or more), e.g.: 20/20 to 20/80

- Blurred vision: Those with nonexudative macular degeneration may be asymptomatic or notice a gradual loss of central vision, whereas those with exudative macular degeneration often notice a rapid onset of vision loss (often caused by leakage and bleeding of abnormal blood vessels).

- Trouble discerning colors, specifically dark ones from dark ones and light ones from light ones

- A loss in contrast sensitivity

Macular degeneration by itself will not lead to total blindness. For that matter, only a very small number of people with visual impairment are totally blind. In almost all cases, some vision remains, mainly peripheral. Other complicating conditions may possibly lead to such an acute condition (severe stroke or trauma, untreated glaucoma, etc.), but few macular degeneration patients experience total visual loss.

The area of the macula comprises only about 2.1% of the retina, and the remaining 97.9% (the peripheral field) remains unaffected by the disease. Even though the macula provides such a small fraction of the visual field, almost half of the visual cortex is devoted to processing macular information.

The loss of central vision profoundly affects visual functioning. It is quite difficult, for example, to read without central vision. Pictures that attempt to depict the central visual loss of macular degeneration with a black spot do not really do justice to the devastating nature of the visual loss. This can be demonstrated by printing letters six inches high on a piece of paper and attempting to identify them while looking straight ahead and holding the paper slightly to the side. Most people find this difficult to do.

A rhegmatogenous retinal detachment is commonly preceded by a posterior vitreous detachment which gives rise to these symptoms:

- flashes of light (photopsia) – very brief in the extreme peripheral (outside of center) part of vision

- a sudden dramatic increase in the number of floaters

- a ring of floaters or hairs just to the temporal (skull) side of the central vision

Although most posterior vitreous detachments do not progress to retinal detachments, those that do produce the following symptoms:

- a dense shadow that starts in the peripheral vision and slowly progresses towards the central vision

- the impression that a veil or curtain was drawn over the field of vision

- straight lines (scale, edge of the wall, road, etc.) that suddenly appear curved (positive Amsler grid test)

- central visual loss

In the event of an appearance of sudden flashes of light or floaters, an eye doctor needs to be consulted immediately. A shower of floaters or any loss of vision, too, is a medical emergency.

Patients with Stargardt disease usually develop symptoms in the mid-first to the late second decade of life, with age of onset which can be as early as ~6 years of age. The main symptom of Stargardt disease is loss of visual acuity, uncorrectable with glasses, which progresses and frequently stabilizes between 20/200 and 20/400. Other symptoms include wavy vision, blind spots (scotomata), blurriness, impaired color vision, and difficulty adapting to dim lighting (delayed dark adaptation). The disease sometimes causes sensitivity to glare; overcast days offer some relief. Vision is most noticeably impaired when the macula (center of retina and focus of vision) is damaged, leaving peripheral vision more intact. Generally, vision loss starts within the first 20 years of life.

Examination with an ophthalmoscope shows few notable findings in the early stages of the disease. Eventually, however, an oval-shaped atrophy with a horizontal major axis appears in the retinal pigment epithelium, and has the appearance of beaten bronze, along with sparing of the area surrounding the optic disc (peripapillary sparing). Techniques such as fundus autofluorescence (FAF), Optical Coherence Tomography (OCT), or less frequently fluorescein angiography, can detect early signs before they are visible ophthalmoscopically.

Seeing rainbows around lights, especially at night, usually indicates swelling of the cornea. This may occur from a variety of causes which are discussed under Corneal Edema. Cataract can sometimes cause this also.

Colour vision is perceived mainly by the macula, which is the central vision portion of the retina. Thus any disorder affecting the macula may cause a disturbance in color vision. However, about 8% of males and 0.5% of females have some version of "colour blindness" from birth. Usually this is a genetically inherited trait, and is of the "red-green confusion" variety. The reds, browns, olives, and gold may be confused. Purple may be confused with blue, and pastel pinks, oranges, yellows, and greens look similar. Usually both eyes are affected equally.

There are many obscure macular retinal disorders that can lead to a loss of colour vision, and many of these syndromes are inherited as well. There may also be a problem with a generalized loss of vision with these problems as well. Other retinal problems can lead to a temporary disturbance of colour vision, such as Central serous chorioretinopathy, Macular Edema of different causes, and Macular Degeneration.

Certain types of cataract can gradually affect the colour vision, but this is usually not noticed until one cataract is removed. The cataract seems to filter out the colour blue, and everything seems more blue after cataract extraction. Optic nerve disorders such as Optic Neuritis can greatly affect colour vision, with colours seeming washed out during or after an episode.

Vision in the affected eye is impaired, the degree of which depends on the size of the defect, and typically affects the visual field more than visual acuity. Additionally, there is an increased risk of serous retinal detachment, manifesting in 1/3 of patients. If retinal detachment does occur, it is usually not correctable and all sight is lost in the affected area of the eye, which may or may not involve the macula.

Corneal dystrophy may not significantly affect vision in the early stages. However, it does require proper evaluation and treatment for restoration of optimal vision. Corneal dystrophies usually manifest themselves during the first or second decade but sometimes later. It appears as grayish white lines, circles, or clouding of the cornea. Corneal dystrophy can also have a crystalline appearance.

There are over 20 corneal dystrophies that affect all parts of the cornea. These diseases share many traits:

- They are usually inherited.

- They affect the right and left eyes equally.

- They are not caused by outside factors, such as injury or diet.

- Most progress gradually.

- Most usually begin in one of the five corneal layers and may later spread to nearby layers.

- Most do not affect other parts of the body, nor are they related to diseases affecting other parts of the eye or body.

- Most can occur in otherwise totally healthy people, male or female.

Corneal dystrophies affect vision in widely differing ways. Some cause severe visual impairment, while a few cause no vision problems and are diagnosed during a specialized eye examination by an ophthalmologist. Other dystrophies may cause repeated episodes of pain without leading to permanent loss of vision.

Open-angle glaucoma is painless and does not have acute attacks, thus the lack of clear symptoms make screening via regular eye check-ups important. The only signs are gradually progressive visual field loss, and optic nerve changes (increased cup-to-disc ratio on fundoscopic examination).

About 10% of people with closed angles present with acute angle closure characterized by sudden ocular pain, seeing halos around lights, red eye, very high intraocular pressure (>30 mmHg), nausea and vomiting, suddenly decreased vision, and a fixed, mid-dilated pupil. It is also associated with an oval pupil in some cases. Acute angle closure is an emergency.

Opaque specks may occur in the lens in glaucoma, known as glaukomflecken.

Vitelliform macular dystrophy causes a fatty yellow pigment (lipofuscin) to build up in cells underlying the macula. The retinal pigment epithelium also degenerates. Over time, the abnormal accumulation of this substance can damage the cells that are critical for clear central vision. As a result, people with this disorder often lose their central vision and may experience blurry or distorted vision, and loss is rarely symmetric. Scotomata appear, first with red light and then for green; finally, relative (or in more serious cases, absolute) scotomata occur with white light. Vitelliform macular dystrophy does not affect side (peripheral) vision or the ability to see at night.

Researchers have described two forms of vitelliform macular dystrophy with similar features. The early-onset form (known as Best disease) usually appears in childhood; however, the onset of symptoms and the severity of vision loss vary widely. The adult-onset form begins later, usually in middle age, and tends to cause relatively mild vision loss. The two forms of vitelliform macular dystrophy each have characteristic changes in the macula that can be detected during an eye examination.

Distortion of vision refers to straight lines not appearing straight, but instead bent, crooked, or wavy. Usually this is caused by distortion of the retina itself. This distortion can herald a loss of vision in macular degeneration, so anyone with distorted vision should seek medical attention by an ophthalmologist promptly. Other conditions leading to swelling of the retina can cause this distortion, such as macular edema and central serous chorioretinopathy.

An Amsler grid can be supplied by an ophthalmologist so that the vision can be monitored for distortion in people who may be predisposed to this problem.

Tunnel vision implies that the peripheral vision, or side vision, is lost, while the central vision remains. Thus, the vision is like looking through a tunnel, or through a paper towel roll. Some disorders that can cause this include:

Glaucoma - severe glaucoma can result in loss of nearly all of the peripheral vision, with a small island of central vision remaining. Sometimes even this island of vision can be lost as well.

Retinitis pigmentosa - This is usually a hereditary disorder which can be part of numerous syndromes. It is more common in males. The peripheral retina develops pigmentary deposits, and the peripheral vision gradually becomes worse and worse. The central vision can be affected eventually as well. People with this problem may have trouble getting around in the dark. Cataract can be a complication as well. There is no known treatment for this disorder, and supplements of Vitamin A have not been proven to help.

Punctate Inner Choroidopathy - This condition is where vessels gro (( material is missing ))

Stroke - a stroke involving both sides of the visual part of the brain may wipe out nearly all of the peripheral vision. Fortunately, this is a very rare occurrence

Retinoschisis is an eye disease characterized by the abnormal splitting of the retina's neurosensory layers, usually in the outer plexiform layer. Most common forms are asymptomatic, some rarer forms result in a loss of vision in the corresponding visual field.

A corneal dystrophy can be caused by an accumulation of extraneous material in the cornea, including lipids and cholesterol crystals.

The most prominent symptoms of Norrie disease are ocular. The first visible finding is leukocoria, a grayish-yellow pupillary reflex that originates from a mass of unorganized tissue behind the lens. This material, which possibly includes an already detached retina, may be confused with a tumor and thus is termed pseudoglioma. However, an affected baby may have a normally sized eye globe and inconspicuous iris, anterior chamber, cornea and intraocular pressure.

Over the first few months of life, complete or partial retinal detachment evolves. From infancy through childhood, the patient may undergo progressive changes in the disease. These progressions include the formation of cataracts, deterioration of the iris with adhesions forming between the iris and the lens or the cornea, and shallowing of the anterior chamber which may increase intraocular pressure, causing eye pain. As the situation worsens, there is corneal opacification, where the cornea becomes opaque, and band keratopathy. Intraocular pressure is lost and the globe shrinks. In the last stage of Norrie disease, the globes appear small and sunken in (phthisis bulbi) and the cornea appears to be milky .

Norrie disease can also have cognitive and behavioral symptoms. Developmental delay or learning difficulties are present in about 30 to 50% of males who have Norrie disease. Psychotic-like features and poorly characterized behavior abnormalities may also be present. Auditory symptoms are common with Norrie disease. Progressive hearing loss starts in early childhood for a majority of males with the condition. Early hearing loss is sensorineural, mild and asymmetric. By adolescence, high-frequency hearing loss begins to appear. Hearing loss is severe, symmetric, and broad-spectrum by the age of 35. However, studies show that while the hearing loss is deteriorating, the ability to speak well is highly preserved. The slowly progressing hearing loss is more problematic to adjust to than the congenital blindness for most people with Norrie disease.

Macular telangiectasia describes two distinct retinal diseases affecting the macula of the eye, macular telangiectasia type 1 and macular telangiectasia type 2.

Macular telangiectasia (MacTel) type 1 is a very rare disease, typically unilateral and usually affecting male patients. MacTel type 2 is more frequent than type 1 and generally affects both eyes (bilateral). It usually affects both sexes equally. Both types of MacTel should not be confused with Age-related macular degeneration (AMD), from which it can be distinguished by symptoms, clinical features, pathogenesis, and disease management. However, both AMD and MacTel eventually lead to (photoreceptor) atrophy and thus loss of central vision.

The etiology of both types of MacTel is still unknown and no treatment has been found to be effective to prevent further progression. Because lost photoreceptors cannot be recovered, early diagnosis and treatment appear to be essential to prevent loss of visual function. Several centers are currently trying to find new diagnostics and treatments to understand the causes and biochemical reactions in order to halt or counteract the adverse effects.

Contemporary research has shown that MacTel type 2 is likely a neurodegenerative disease with secondary changes of the blood vessels of the macula. Although MacTel type 2 has been previously regarded as a rare disease, it is in fact probably much more common than previously thought. The very subtle nature of the early findings in MacTel mean the diagnoses are often missed by optometrists and general ophthalmologists. Due to increased research activity since 2005, many new insights have been gained into this condition since its first description by Dr. J. Donald Gass in 1982.

This type of retinoschisis is very common with a prevalence of up to 7 percent in normal persons. Its cause is unknown. It can easily be confused with retinal detachment by the non-expert observer and in difficult cases even the expert may have difficulty differentiating the two. Such differentiation is important since retinal detachment almost always requires treatment while retinoschisis never itself requires treatment and leads to retinal detachment (and hence to visual loss) only occasionally. Unfortunately one still sees cases of uncomplicated retinoschisis treated by laser retinopexy or cryopexy in an attempt to stop its progression towards the macula. Such treatments are not only ineffective but unnecessarily risk complications. There is no documented case in the literature of degenerative retinoschisis itself (as opposed to the occasional situation of retinal detachment complicating retinoschisis) in which the splitting of the retina has progressed through the fovea. There is no clinical utility in differentiating between typical and reticular retinoschisis. Degenerative retinoschisis is not known to be a genetically inherited condition.

There is always vision loss in the region of the schisis as the sensory retina is separated from the ganglion layer. But like the loss is in the periphery, it goes unnoticed. It is the very rare schisis that encroaches on the macula where retinopexy is then properly used.

The first noticeable signs of the syndrome usually do not appear until after the first twelve months of the child’s life. The child usually has severe balance issues as he or she learns to sit or walk, often leaning or tilting the head toward the good eye to correct the brain’s skewed perception of the world. Often the child will fall in the same direction while walking or run into objects that are placed on his or her blind side. Additionally, family members may notice a white reflex in the pupil of an affected child instead of the normal red reflex when taking photographs. The presence of this phenomenon is dependent on the degree of the coloboma, with larger colobomas more likely to manifest this particular phenomenon.

This anomaly must be confirmed through pupillary dilation and examination of the optic disc, as the symptoms alone do not constitute a diagnosis.

People with optic nerve colobomas live relatively normal lives. Although non-prescription glasses should be worn for eye protection, this syndrome does not usually prevent the individual from living a normal life, driving cars, playing sports, reading, etc. Certain activities, however, may be more difficult for patients with optic nerve colobomas due to a compromised view of the world. Like most other eye conditions, a diagnosis of optic nerve coloboma precludes a person from certain occupations.