Typical symptoms of dry eye syndrome are dryness, burning and a sandy-gritty eye irritation that gets worse as the day goes on. Symptoms may also be described as itchy, scratchy, stinging or tired eyes. Other symptoms are pain, redness, a pulling sensation, and pressure behind the eye. There may be a feeling that something, such as a speck of dirt, is in the eye. The resultant damage to the eye surface increases discomfort and sensitivity to bright light. Both eyes usually are affected.

There may also be a stringy discharge from the eyes. Although it may seem strange, dry eye can cause the eyes to water. This can happen because the eyes are irritated. One may experience excessive tearing in the same way as one would if something got into the eye. These reflex tears will not necessarily make the eyes feel better. This is because they are the watery type that are produced in response to injury, irritation, or emotion. They do not have the lubricating qualities necessary to prevent dry eye.

Because blinking coats the eye with tears, symptoms are worsened by activities in which the rate of blinking is reduced due to prolonged use of the eyes. These activities include prolonged reading, computer usage, driving, or watching television. Symptoms increase in windy, dusty or smoky (including cigarette smoke) areas, in dry environments high altitudes including airplanes, on days with low humidity, and in areas where an air conditioner (especially in a car), fan, heater, or even a hair dryer is being used. Symptoms reduce during cool, rainy, or foggy weather and in humid places, such as in the shower.

Most people who have dry eyes experience mild irritation with no long-term effects. However, if the condition is left untreated or becomes severe, it can produce complications that can cause eye damage, resulting in impaired vision or (rarely) in the loss of vision.

Symptom assessment is a key component of dry eye diagnosis – to the extent that many believe dry eye syndrome to be a symptom-based disease. Several questionnaires have been developed to determine a score that would allow for dry eye diagnosis. The McMonnies & Ho dry eye questionnaire is often used in clinical studies of dry eyes.

Any abnormality of any one of the three layers of tears produces an unstable tear film, resulting in symptoms of dry eyes.

Corneal ulcers are extremely painful due to nerve exposure, and can cause tearing, squinting, and vision loss of the eye. There may also be signs of anterior uveitis, such as miosis (small pupil), aqueous flare (protein in the aqueous humour), and redness of the eye. An axon reflex may be responsible for uveitis formation—stimulation of pain receptors in the cornea results in release inflammatory mediators such as prostaglandins, histamine, and acetylcholine.

Sensitivity to light (photophobia) is also a common symptom of corneal ulcer.

Measurement of the degree of exophthalmos is performed using an exophthalmometer.

Most sources define exophthalmos/proptosis as a protrusion of the globe greater than 18 mm.

The term exophthalmos is often used when describing proptosis associated with Graves' disease.

Proptosis is the anterior displacement of the eye from the orbit. Since the orbit is closed off posteriorly, medially and laterally, any enlargement of structures located within will cause the anterior displacement of the eye. Swelling or enlargement of the lacrimal gland causes inferior medial and anterior dislocation of the eye. This is because the lacrimal glands are located superiorly and laterally in the orbit.

Red eye, swelling of conjunctiva and watering of the eyes are symptoms common to all forms of conjunctivitis. However, the pupils should be normally reactive, and the visual acuity normal.

Viral conjunctivitis is often associated with an infection of the upper respiratory tract, a common cold, or a sore throat. Its symptoms include excessive watering and itching. The infection usually begins with one eye, but may spread easily to the other.

Viral conjunctivitis shows a fine, diffuse pinkness of the conjunctiva, which is easily mistaken for the ciliary infection of iris (iritis), but there are usually corroborative signs on microscopy, particularly numerous lymphoid follicles on the tarsal conjunctiva, and sometimes a punctate keratitis.

Keratoconjunctivitis is inflammation ("-itis") of the cornea and conjunctiva.

When only the cornea is inflamed, it is called "keratitis"; when only the conjunctiva is inflamed, it is called "conjunctivitis".

There are several potential causes of the inflammation:

- Keratoconjunctivitis sicca is used when the inflammation is due to dryness. ("Sicca" means "dryness" in medical contexts.) It occurs with 20% of rheumatoid arthritis patients.

- The term "Vernal keratoconjunctivitis" (VKC) is used to refer to keratoconjunctivitis occurring in spring, and is usually considered to be due to allergens.

- "Atopic keratoconjunctivitis" is one manifestation of atopy.

- "Epidemic keratoconjunctivitis" is caused by an adenovirus infection.

- "Infectious bovine keratoconjunctivitis" (IBK) is a disease affecting cattle caused by the bacteria "Moraxella bovis".

- "Pink eye in sheep and goat" is another infectious keratoconjunctivitis of veterinary concern, mostly caused by "Chlamydophila pecorum"

- "Superior limbic keratoconjunctivitis" is thought to be caused by mechanical trauma.

- "Keratoconjunctivitis photoelectrica" (arc eye) means inflammation caused by photoelectric UV light. It is a type of ultraviolet keratitis. Such UV exposure can be caused by arc welding without wearing protective eye glass, or by high altitude exposure from sunlight reflected from snow ("snow blindness"). The inflammation will only appear after about 6 to 12 hours. It can be treated by rest, as the inflammation usually heals after 24–48 hours. Proper eye protection should be worn to prevent keratoconjunctivitis photoelectrica.

Cherry eye is most common in young dogs, especially breeds such as Cavalier King Charles Spaniel, English Bulldog, Lhasa Apso, Shih Tzu, West Highland White Terrier, Pug, Bloodhound, American Cocker Spaniel, and Boston Terrier Cherry eye is rare in felines, but can occur. This defect is most common in the Burmese breed of felines. A similar condition exists in dwarf lop-eared rabbits, which occurs in the harderian gland. Similar surgical treatment is necessary.

Cherry eye is not considered a genetic problem, as no proof of inheritance has been determined. The NM contains many glands which merge and appear as a single gland. Typically, glands secrete tears for lubrication of the cornea. Lack of anchoring allows the gland to flip up, causing the gland to prolapse.

Symptoms include a visible fleshy mass, abnormal tear production, and a discharge or drainage from the eye. Cherry eye is typically diagnosed by examination of the conjunctiva and nictitating membrane. The most obvious symptom of cherry eye is a round fleshy mass through medial canthus of the eye, similar in appearance to the fruit it is named for. This mass may be unilateral or ‘’bilateral’’. Both eyes may develop cherry eye at different times in the animal’s life. Other symptoms of cherry eye include drainage from the eye and abnormal tear production. Initially, cherry eye results in overproduction of tears, but eventually changes to unsubstantial tear production.

Cherry eye is a disorder of the nictitating membrane (NM), also called the third eyelid, present in the eyes of dogs and cats. Cherry eye is most often seen in young dogs under the age of two. Common misnomers include adenitis, hyperplasia, adenoma of the gland of the third eyelid; however, cherry eye is not caused by hyperplasia, neoplasia, or primary inflammation. In many species, the third eyelid plays an essential role in vision by supplying oxygen and nutrients to the eye via tear production. Normally, the gland can evert without detachment. Cherry eye results from a defect in the retinaculum which is responsible for anchoring the gland to the periorbita. This defect causes the gland to prolapse and protrude from the eye as a red fleshy mass. Problems arise as sensitive tissue dries out and is subjected to external trauma Exposure of the tissue often results in secondary inflammation, swelling, or infection. If left untreated, this condition can lead to Keratoconjunctivitis sicca (KCS) and other complications.

Corneal ulcers are a common human eye disease. They are caused by trauma, particularly with vegetable matter, as well as chemical injury, contact lenses and infections. Other eye conditions can cause corneal ulcers, such as entropion, distichiasis, corneal dystrophy, and keratoconjunctivitis sicca (dry eye).

Many micro-organisms cause infective corneal ulcer. Among them are bacteria, fungi, viruses, protozoa, and chlamydia:

- Bacterial keratitis is caused by "Staphylococcus aureus", "Streptococcus viridans", "Escherichia coli", "Enterococci", "Pseudomonas", "Nocardia", "N. Gonorrhoea" and many other bacteria.

- Fungal keratitis causes deep and severe corneal ulcer. It is caused by "Aspergillus" sp., "Fusarium" sp., "Candida" sp., as also "Rhizopus", "Mucor", and other fungi. The typical feature of fungal keratitis is slow onset and gradual progression, where signs are much more than the symptoms. Small satellite lesions around the ulcer are a common feature of fungal keratitis and hypopyon is usually seen.

- Viral keratitis causes corneal ulceration. It is caused most commonly by Herpes simplex, Herpes zoster and Adenoviruses. Also it can be caused by coronaviruses & many other viruses. Herpes virus cause a dendritic ulcer, which can recur and relapse over the lifetime of an individual.

- Protozoa infection like "Acanthamoeba keratitis" is characterized by severe pain and is associated with contact lens users swimming in pools.

- "Chlamydia trachomatis" can also contribute to development of corneal ulcer.

Superficial ulcers involve a loss of part of the epithelium. Deep ulcers extend into or through the stroma and can result in severe scarring and corneal perforation. Descemetoceles occur when the ulcer extends through the stroma. This type of ulcer is especially dangerous and can rapidly result in corneal perforation, if not treated in time.

The location of the ulcer depends somewhat on the cause. Central ulcers are typically caused by trauma, dry eye, or exposure from facial nerve paralysis or exophthalmos. Entropion, severe dry eye and trichiasis (inturning of eyelashes) may cause ulceration of the peripheral cornea. Immune-mediated eye disease can cause ulcers at the border of the cornea and sclera. These include Rheumatoid arthritis, rosacea, systemic sclerosis which lead to a special type of corneal ulcer called Mooren's ulcer. It has a circumferential crater like depression of the cornea, just inside the limbus, usually with an overhanging edge.

Oculomucocutaneous syndrome is characterized by keratoconjunctivitis sicca and by scarring, fibrosis, metaplasia, and shrinkage of the conjunctiva. It is a drug side effect observed in practolol and eperisone. It is speculated that antibodies against drug metabolites cause the syndrome.

Dryness is a medical condition in which there is local or more generalized decrease in normal lubrication of the skin or mucous membranes.

Examples of local dryness include dry mouth, dry eyes, dry skin and vaginal dryness. These often have specific causes and treatments. It is possible to have dry eyes without any other signs or symptoms, but this usually causes a syndrome of eye symptoms called keratoconjunctivitis sicca.

More generalized dryness can be caused by e.g. dehydration (that is, more general loss of body fluids), anticholinergic drugs and Sjögren syndrome.

The experience of amaurosis fugax is classically described as a temporary loss of vision in one or both eyes that appears as a black "curtain coming down vertically into the field of vision in one eye;" however, this altitudinal visual loss is relatively uncommon. In one study, only 23.8 percent of patients with transient monocular vision loss experienced the classic "curtain" or "shade" descending over their vision. Other descriptions of this experience include a monocular blindness, dimming, fogging, or blurring. Total or sectorial vision loss typically lasts only a few seconds, but may last minutes or even hours. Duration depends on the cause of the vision loss. Obscured vision due to papilledema may last only seconds, while a severely atherosclerotic carotid artery may be associated with a duration of one to ten minutes. Certainly, additional symptoms may be present with the amaurosis fugax, and those findings will depend on the cause of the transient monocular vision loss.

Ocular causes include:

- Iritis

- Keratitis

- Blepharitis

- Optic disc drusen

- Posterior vitreous detachment

- Closed-angle glaucoma

- Transient elevation of intraocular pressure

- Intraocular hemorrhage

- Coloboma

- Myopia

- Orbital hemangioma

- Orbital osteoma

- Keratoconjunctivitis sicca

Chronic atrophic rhinitis is a chronic inflammation of nose characterised by atrophy of nasal mucosa, including the glands, turbinate bones and the nerve elements supplying the nose. Chronic atrophic rhinitis may be primary and secondary. Special forms of chronic atrophic rhinitis are rhinitis sicca anterior and ozaena.

Permanent loss of smell and impairment of taste may also be a result of this disease, even after the symptoms are cured.

The hallmark symptom of SS is a generalized dryness, typically including dry mouth and keratoconjunctivitis sicca (dry eyes), part of what are known as sicca ("dryness") symptoms. Sicca syndrome also incorporates vaginal dryness and chronic bronchitis. SS may cause skin, nose, and vaginal dryness, and may affect other organs of the body, including the muscles (myositis), kidneys, blood vessels, lungs, liver, biliary system, pancreas, peripheral nervous system (distal axonal neuropathy or small fiber peripheral neuropathy) and brain. Some people have gastrointestinal or esophageal diseases such as GERD, achlorhydria or gastroparesis. Chronic pain with accompanying fatigue and brain fog may also occur.

Skin dryness in some people with SS may be the result of lymphocytic infiltration into skin glands. The symptoms may develop insidiously, with the diagnosis often not considered for several years, because the complaints of sicca may be otherwise attributed to medications, a dry environment, aging, or may be regarded as not of severity warranting the level of investigation necessary to establish the presence of the specific underlying autoimmune disorder.

SS can damage vital organs of the body with symptoms that may plateau or worsen, or go into remission as with other autoimmune diseases. Some people may experience only the mild symptoms of dry eyes and mouth, while others have symptoms of severe disease. Many patients can treat problems symptomatically. Others are forced to cope with blurred vision, constant eye discomfort, recurrent mouth infections, swollen parotid glands, dysphonia (vocal disorders including hoarseness), and difficulty in swallowing and eating. Debilitating fatigue and joint pain can seriously impair quality of life. Some patients can develop renal (kidney) involvement (autoimmune tubulointerstitial nephritis) leading to proteinuria (excess protein in urine), urinary concentrating defect, and distal renal tubular acidosis.

Individuals with Stickler syndrome experience a range of signs and symptoms. Some people have no signs and symptoms; others have some or all of the features described below. In addition, each feature of this syndrome may vary from subtle to severe.

A characteristic feature of Stickler syndrome is a somewhat flattened facial appearance. This is caused by underdeveloped bones in the middle of the face, including the cheekbones and the bridge of the nose. A particular group of physical features, called the Pierre Robin sequence, is common in children with Stickler syndrome. Robin sequence includes a U-shaped or sometimes V-shaped cleft palate (an opening in the roof of the mouth) with a tongue that is too large for the space formed by the small lower jaw. Children with a cleft palate are also prone to ear infections and occasionally swallowing difficulties.

Many people with Stickler syndrome are very nearsighted (described as having high myopia) because of the shape of the eye. People with eye involvement are prone to increased pressure within the eye (ocular hypertension) which could lead to glaucoma and tearing or detachment of the light-sensitive retina of the eye (retinal detachment). Cataract may also present as an ocular complication associated with Stickler's Syndrome. The jelly-like substance within the eye (the vitreous humour) has a distinctive appearance in the types of Stickler syndrome associated with the COL2A1 and COL11A1 genes. As a result, regular appointments to a specialist ophthalmologist are advised. The type of Stickler syndrome associated with the COL11A2 gene does not affect the eye.

People with this syndrome have problems that affect things other than the eyes and ears. Arthritis, abnormality to ends of long bones, vertebrae abnormality, curvature of the spine, scoliosis, joint pain, and double jointedness are all problems that can occur in the bones and joints. Physical characteristics of people with Stickler can include flat cheeks, flat nasal bridge, small upper jaw, pronounced upper lip groove, small lower jaw, and palate abnormalities, these tend to lessen with age and normal growth and palate abnormalities can be treated with routine surgery.

Another sign of Stickler syndrome is mild to severe hearing loss that, for some people, may be progressive (see hearing loss with craniofacial syndromes). The joints of affected children and young adults may be very flexible (hypermobile). Arthritis often appears at an early age and worsens as a person gets older. Learning difficulties, not intelligence, can also occur because of hearing and sight impairments if the school is not informed and the student is not assisted within the learning environment.

Stickler syndrome is thought to be associated with an increased incidence of mitral valve prolapse of the heart, although no definitive research supports this.

The differential of hyposalivation significantly overlaps with that of xerostomia. A reduction in saliva production to about 50% of the normal unstimulated level will usually result in the sensation of dry mouth. Altered saliva composition may also be responsible for xerostomia.

Heerfordt syndrome, also referred to as uveoparotid fever, Heerfordt–Mylius syndrome, Heerfordt–Waldenström syndrome, and Waldenström's uveoparotitis, is a rare manifestation of sarcoidosis. The symptoms include inflammation of the eye (uveitis), swelling of the parotid gland, chronic fever, and in some cases, of the facial nerves.

True hyposalivation may give the following signs and symptoms:

- Dental caries (xerostomia related caries) – Without the anticariogenic actions of saliva, tooth decay is a common feature and may progress much more aggressively than it would otherwise ("rampant caries"). It may affect tooth surfaces that are normally spared, e.g., cervical caries and root surface caries. This is often seen in patients who have had radiotherapy involving the major salivary glands, termed radiation-induced caries.

- Acid erosion. Saliva acts as a buffer and helps to prevent demineralization of teeth.

- Oral candidiasis – A loss of the antimicrobial actions of saliva may also lead to opportunistic infection with "Candida" species.

- Ascending (suppurative) sialadenitis – an infection of the major salivary glands (usually the parotid gland) that may be recurrent. It is associated with hyposalivation, as bacteria are able to enter the ductal system against the diminished flow of saliva. There may be swollen salivary glands even without acute infection, possibly caused by autoimmune involvement.

- Dysgeusia – altered taste sensation (e.g., a metallic taste) and dysosmia, altered sense of smell.

- Intraoral halitosis – possibly due to increased activity of halitogenic biofilm on the posterior dorsal tongue (although dysgeusia may cause a complaint of nongenuine halitosis in the absence of hyposalivation).

- Oral dysesthesia – a burning or tingling sensation in the mouth.

- Saliva that appears thick or ropey.

- Mucosa that appears dry.

- A lack of saliva pooling in the floor of the mouth during examination.

- Dysphagia – difficulty swallowing and chewing, especially when eating dry foods. Food may stick to the tissues during eating.

- The tongue may stick to the palate, causing a clicking noise during speech, or the lips may stick together.

- Gloves or a dental mirror may stick to the tissues.

- Fissured tongue with atrophy of the filiform papillae and a lobulated, erythematous appearance of the tongue.

- Saliva cannot be "milked" (expressed) from the parotid duct.

- Difficulty wearing dentures, e.g., when swallowing or speaking. There may be generalized mucosal soreness and ulceration of the areas covered by the denture.

- Mouth soreness and oral mucositis.

- Lipstick or food may stick to the teeth.

- A need to sip drinks frequently while talking or eating.

- Dry, sore, and cracked lips and angles of mouth.

- Thirst.

However, sometimes the clinical findings do not correlate with the symptoms experienced. E.g., a person with signs of hyposalivation may not complain of xerostomia. Conversely a person who reports experiencing xerostomia may not show signs of reduced salivary secretions (subjective xerostomia). In the latter scenario, there are often other oral symptoms suggestive of oral dysesthesia ("burning mouth syndrome"). Some symptoms outside the mouth may occur together with xerostomia.

These include:

- Xerophthalmia (dry eyes).

- Inability to cry.

- Blurred vision.

- Photophobia (light intolerance).

- Dryness of other mucosae, e.g., nasal, laryngeal, and/or genital.

- Burning sensation.

- Itching or grittiness.

- Dysphonia (voice changes).

There may also be other systemic signs and symptoms if there is an underlying cause such as Sjögren's syndrome, for example, joint pain due to associated rheumatoid arthritis.

In patients that have already been diagnosed with sarcoidosis, Heerfordt syndrome can be inferred from the major symptoms of the syndrome, which include parotitis, fever, and facial nerve palsy. In cases of parotitis, ultrasound-guided biopsy is used to exclude the possibility of lymphoma. There are many possible causes of facial nerve palsy, including Lyme disease, HIV, Melkersson–Rosenthal syndrome, schwannoma, and Bell's palsy. Heerfordt syndrome exhibits spontaneous remission. Treatments for sarcoidosis include corticosteroids and immunosuppressive drugs.

Although symptoms of AAG can range from patient to patient, hallmark symptoms include:

- gastrointestinal dysmotility

- anhidrosis (decreased ability to sweat)

- bladder dysfunction (neurogenic bladder)

- small fiber peripheral neuropathy

- Severe orthostatic hypotension

- Pupillary dysfunction

- syncope (fainting)

- Sicca syndrome (chronic dryness of the eyes and mouth)

SS is associated with a number of other medical conditions, many of which are autoimmune or rheumatic disorders, such as celiac disease, fibromyalgia, SLE (lupus), autoimmune thyroiditis, multiple sclerosis and spondyloarthropathy, and several malignancies, principally non-Hodgkin lymphoma.