Eye structures and visual disturbances that occur when they are affected

 

The Pupil: Size, Reactivity, and Pathological Changes

The pupil is the central aperture of the iris that controls the amount of light entering the eye. Its size is dynamically regulated by the interplay of the sphincter pupillae muscle (parasympathetically innervated, causes constriction/miosis) and the dilator pupillae muscle (sympathetically innervated, causes dilation/mydriasis). Pupil size and reactivity to light and accommodation (near focusing) are important indicators of the integrity of ocular innervation and can provide clues to various pathological conditions.

 

Anisocoria: Physiological vs. Pathological

A slight, normal asymmetry in pupil size between the two eyes (up to 1mm difference) is called physiological anisocoria and can occur in some healthy individuals. In such cases, pupillary reactions to light and accommodation are preserved and symmetrical.

Pathological anisocoria refers to unequal pupil sizes due to an underlying disease process affecting the sympathetic or parasympathetic innervation of the eye, or structural abnormalities of the iris.

• Lesions of Sympathetic Innervation (Horner's Syndrome): Characterized by a triad of miosis (constricted pupil) on the affected side, partial ptosis (drooping of the upper eyelid due to paralysis of Müller's muscle), and facial anhidrosis (decreased sweating) on the same side. The constricted pupil in Horner's syndrome still reacts to light and accommodation, though dilation in dim light is impaired.
• Lesions of Parasympathetic Innervation (e.g., Oculomotor Nerve - CN III - Palsy, Adie's Tonic Pupil):
  • Internal Ophthalmoplegia (CN III Palsy affecting parasympathetics): Manifests as a dilated pupil (mydriasis) with no or a weak reaction to light. Accommodation may also be impaired. Instillation of a weak (e.g., 0.125%) pilocarpine solution can cause constriction in cases of denervation supersensitivity (Adie's pupil), while a 1% pilocarpine solution is used to distinguish pharmacological blockade (e.g., from atropine, which will not constrict) from true nerve palsy (which will constrict). Local application of pilocarpine in various concentrations helps the physician differentiate CN III palsy from mydriasis caused by anticholinergic drugs (like atropine, where the pupil won't constrict even to strong pilocarpine) or from Adie's tonic pupil. Adie's pupil is typically unilateral, dilated, reacts poorly or slowly to light but shows a slow, tonic constriction with near effort (light-near dissociation), and often redilates slowly. It's often associated with diminished deep tendon reflexes (Holmes-Adie syndrome).
• Argyll Robertson Pupil: Typically bilateral small, irregular pupils that do not react to light but constrict normally with accommodation and convergence ("light-near dissociation"). Classically associated with neurosyphilis, but can also be seen in other conditions like diabetes or midbrain lesions.
• Structural Iris Damage: Trauma, inflammation (iritis), or previous surgery can damage the iris muscles, leading to irregular pupil shape or impaired reactivity.

Observing pupil size, shape, symmetry, and reactions to light (direct and consensual) and near stimulus is a critical part of the neurological and ophthalmological examination to detect impaired innervation or local eye disease.

 

Intraocular Fluid Dynamics and Glaucoma

Glaucoma is a group of eye diseases characterized by progressive damage to the optic nerve, often (but not always) associated with an increase in intraocular pressure (IOP). This optic nerve damage leads to characteristic patterns of visual field loss and can result in irreversible blindness if untreated.

 

Intraocular Pressure (IOP) and its Regulation

Intraocular fluid, specifically the aqueous humor, is a clear fluid that fills the anterior and posterior chambers of the eye. It is continuously produced by the ciliary epithelium of the ciliary body. Aqueous humor provides essential nutrients and maintains metabolic homeostasis for avascular structures of the eye like the lens and cornea. The level of IOP is determined by the dynamic balance between the rate of aqueous humor production and the resistance to its outflow from the eye. Aqueous humor flows from the posterior chamber, through the pupil, into the anterior chamber, and then primarily exits the eye through the trabecular meshwork located in the angle of the anterior chamber, into Schlemm's canal, and finally into the episcleral venous system (venous collectors). A smaller portion exits via the uveoscleral outflow pathway.

In most cases, the cause of glaucoma is not an increased production of intraocular fluid, but rather an impaired or obstructed outflow of aqueous humor from the anterior chamber of the eye.

 

Pathophysiology of Glaucomatous Optic Neuropathy

Elevated IOP is a major risk factor for glaucoma. Increased pressure within the eye can lead to mechanical stress and compromised blood flow (ischemia) at the optic nerve head, causing damage and death of retinal ganglion cell axons that form the optic nerve. This results in a characteristic cupping (excavation) of the optic disc and progressive thinning of the retinal nerve fiber layer.

Glaucoma is a leading cause of irreversible blindness worldwide. It is estimated to affect about 1 in 50 people over the age of 35, with prevalence increasing with age. A significant portion of the population may have glaucoma without being aware of it, as early stages (especially of open-angle glaucoma) are often asymptomatic. Therefore, routine eye examinations that include IOP measurement and optic disc evaluation are crucial for early detection, similar to how blood pressure measurement is a necessary component of general medical examinations for adults.

Measurement of IOP (tonometry) is a key part of an ophthalmological examination. IOP is considered elevated if it is consistently above 21-22 mm Hg (Schiøtz tonometry was a historical method; Goldmann applanation tonometry is the current gold standard, with non-contact tonometry used for screening).

Patients with glaucoma can have significant daily fluctuations in IOP, sometimes falling within the normal range during a single measurement. Thus, it is very important to examine the optic discs for characteristic glaucomatous changes (increased cupping, asymmetry between eyes, notching of the neuroretinal rim, nerve fiber layer defects) and to perform visual field testing (perimetry) to detect typical patterns of visual field loss (e.g., arcuate scotomas, nasal step). Visual field loss typically follows the progressive cupping and damage of the optic disc. Asymmetry of the optic nerve discs between the two eyes can be an early diagnostic sign of glaucoma. With the progression of optic nerve damage, irreversible death of nerve tissue occurs, leading to changes in the disc's contour (excavation or depression) and color (pallor from atrophy).

 

Types of Glaucoma

The main types of glaucoma that affect the human eye include primary and secondary forms:

 

Open-Angle Glaucoma (Primary Open-Angle Glaucoma - POAG)

POAG arises as a result of chronic difficulty in the reabsorption (outflow) of aqueous humor through the trabecular meshwork, despite the anterior chamber angle appearing open on gonioscopy (direct examination of the angle structures). POAG is usually asymptomatic in its early stages ("silent thief of sight"). Only in rare cases, with very high IOP, might pain in the eyeball or corneal edema (causing halos around lights) develop. Peripheral visual fields are typically lost first, while central visual acuity often remains normal until the later stages of the disease.

The diagnosis of POAG is based on detecting elevated IOP (though some patients have normal-tension glaucoma), characteristic optic disc cupping, retinal nerve fiber layer defects, and corresponding visual field loss. Management tactics for early-stage POAG often involve regular re-examinations with repeated IOP measurements, visual field testing, and thorough fundus examinations (including OCT imaging) to monitor for progression of optic disc cupping and nerve fiber layer thinning.

Treatment of POAG begins with conservative medical methods aimed at lowering IOP. Topical medications include:

• Prostaglandin analogs (e.g., latanoprost, travoprost, bimatoprost) - increase uveoscleral outflow.
• Beta-blockers (e.g., timolol, betaxolol) - reduce aqueous humor production.
• Alpha-adrenergic agonists (e.g., brimonidine, apraclonidine) - decrease production and increase outflow.
• Carbonic anhydrase inhibitors (topical e.g., dorzolamide, brinzolamide; or oral e.g., acetazolamide/diacarb) - reduce aqueous production. Diuretics like acetazolamide can have a positive effect.
• Cholinergic drugs (miotics like pilocarpine or carbacholine) - increase trabecular outflow (less commonly used now as first-line).

In cases where medical therapy is insufficient or not tolerated, laser trabeculoplasty (e.g., SLT, ALT) or surgical procedures are considered. Surgery aims to prevent permanent visual impairment by creating new outflow pathways. Common operations include:

• Trabeculectomy (creating a fistula from the anterior chamber to the subconjunctival space).
• Glaucoma drainage device implantation (shunts/valves).
• Minimally Invasive Glaucoma Surgery (MIGS) procedures.

 

Angle-Closure Glaucoma (Primary Angle-Closure Glaucoma - PACG)

Angle-closure glaucoma develops when aqueous humor outflow is obstructed by the peripheral iris physically blocking or covering the trabecular meshwork, due to a narrow anterior chamber angle. This obstruction to fluid flow can occur suddenly (acute angle-closure crisis) or intermittently/chronically.

• Acute Angle-Closure Crisis: A medical emergency characterized by sudden, severe eye pain, headache, blurred vision, halos around lights, nausea, and vomiting. The eye is often red, the cornea cloudy, and the pupil mid-dilated and non-reactive. IOP is typically very high.
• Chronic Angle-Closure Glaucoma: May be asymptomatic or cause intermittent symptoms. Peripheral anterior synechiae (adhesions between iris and trabecular meshwork) can form, leading to progressive IOP elevation and optic nerve damage. Diagnosis relies on gonioscopy to visualize the narrow or closed angle.

The use of medications that cause pupillary dilation (mydriasis), such as anticholinergics or sympathomimetics, can precipitate an acute angle-closure attack in predisposed individuals with narrow angles. Therefore, in patients over the age of 50, or those with shallow anterior chambers, the anterior chamber angle should be examined by gonioscopy before prescribing drugs that dilate the pupil.

Treatment of acute angle-closure glaucoma requires urgent measures to lower IOP dramatically. This includes:

• Topical miotics (pilocarpine - to constrict pupil and pull iris away from angle, but may be ineffective if IOP is very high).
• Topical beta-blockers, alpha-agonists, and carbonic anhydrase inhibitors.
• Systemic medications: Oral or intravenous acetazolamide, intravenous mannitol (an osmotic diuretic). Parenteral diacarb (acetazolamide) is used.

After urgent medical measures to lower IOP, definitive treatment, usually laser peripheral iridotomy (creating a small hole in the peripheral iris to allow aqueous flow) or surgical iridectomy, is often required to prevent recurrence and create a passage between the anterior and posterior chambers of the eye.

 

Congenital Glaucoma (Primary Congenital Glaucoma)

Congenital glaucoma is a rare type of glaucoma, usually presenting as open-angle, that develops due to abnormal development (dysgenesis) of the aqueous humor outflow structures of the anterior chamber angle (trabecular meshwork). It typically manifests in infancy or early childhood. Congenital glaucoma can cause significant vision loss, enlargement of the eyeball (buphthalmos or "ox eye") due to the distensibility of infant sclera, and corneal damage (clouding, Haab's striae - breaks in Descemet's membrane). Early diagnosis of congenital glaucoma is crucial for prompt surgical treatment (e.g., goniotomy, trabeculotomy) to prevent irreversible blindness. Conservative medical treatment is often adjunctive or temporizing.

 

Secondary Glaucoma

Secondary glaucoma develops as a complication of another systemic disease already existing in the patient or as a result of a local eye lesion or medication use. Numerous conditions can lead to secondary glaucoma:

• Ocular Conditions: Uveitis, eye trauma (causing angle recession or hyphema), intraocular tumors, dislocated lens, advanced cataracts, retinal vascular occlusions leading to neovascular glaucoma.
• Systemic Diseases:
  • Blood diseases (leukemia, sickle cell anemia, Waldenström macroglobulinemia - can cause hyperviscosity or angle blockage).
  • Collagen vascular diseases (ankylosing spondylitis, rheumatoid arthritis, sarcoidosis - associated with uveitis).
  • Skin diseases (allergic reactions, Ota's nevus).
  • Infectious diseases (congenital rubella, onchocerciasis).
  • Metabolic disorders (amyloidosis, Marchesani syndrome).
  • Skeletal muscle lesions (Conradi's disease, osteogenesis imperfecta - these are broad syndromes, specific link to glaucoma might be through associated ocular anomalies).
  • Neoplasms (metastases to the trabecular meshwork or angle structures).
  • Phakomatoses (neurofibromatosis, Sturge-Weber syndrome).
  • Lung diseases (asthma, emphysema - primarily if leading to corticosteroid use).
  • Kidney damage (Lowe's syndrome - oculo-cerebro-renal syndrome with aminoaciduria; Wilms' tumor - aniridia-Wilms tumor association; kidney transplant - due to corticosteroid use).
• Medications: Prolonged use of corticosteroids (topical, periocular, systemic, or inhaled) is a major cause of steroid-induced glaucoma. Other drugs like phenamine (amphetamine), benzohexonium (hexamethonium - historical antihypertensive), reserpine (historical antihypertensive), and anticholinergics can potentially trigger angle closure in predisposed eyes.

Local eye lesions that can cause secondary glaucoma in a patient include trauma to the eyeball. The development of secondary glaucoma is also possible with dislocation of the lens, which can occur in conditions like homocystinuria or Marfan syndrome.

 

The Lens and Cataracts

A cataract is defined as any opacification or clouding of the normally transparent crystalline lens of the eye. Cataracts can be localized to specific parts of the lens, such as the center (nuclear cataract), the superficial cortical region (cortical cataract), or the posterior subcapsular region (posterior subcapsular cataract - PSC). A cataract develops in response to changes in the physical and chemical properties of the lens environment within its semi-permeable capsule, leading to protein denaturation and aggregation.

 

Formation and Types of Cataracts

By origin, cataracts can be congenital (present at birth or developing in early infancy) or acquired (developing later in life).

• Congenital Cataracts: Can occur due to intrauterine infections during pregnancy, such as:
  • Rubella (Congenital Rubella Syndrome)
  • Herpes simplex
  • Syphilis
  • Cytomegalovirus (CMV)
  • Toxoplasmosis
  Also associated with genetic syndromes (e.g., Down syndrome, Lowe's syndrome) or inherited metabolic disorders (e.g., galactosemia).
• Acquired Cataracts: Result from various factors:
  • Age-Related (Senile Cataract): The most common type, developing as part of the natural aging process.
  • Trauma: Blunt or penetrating injury to the eye.
  • Radiation Exposure: Ionizing radiation or prolonged UV exposure.
  • Drug Use: Prolonged use of corticosteroids (systemic, topical, inhaled), miotics, phenothiazines, amiodarone.
  • Metabolic Disorders: Diabetes mellitus, hypocalcemia, galactosemia, hypoglycemia, Wilson's disease.
  • Other Eye Conditions: Chronic uveitis, high myopia, retinitis pigmentosa.

Two types of cataracts are often described in diabetic patients:

• True Diabetic Cataract (Metabolic or "Snowflake" Cataract): Less common, typically seen in young individuals with poorly controlled, insulin-dependent diabetes. Characterized by bilateral, rapidly progressing snowflake-like or flocculent opacities, often starting in the subcapsular regions. This is related to osmotic changes within the lens due to high glucose levels and sorbitol accumulation.
• Age-Related (Senile) Cataract: Develops at an earlier age and matures faster in individuals with diabetes compared to non-diabetic people.

Other metabolic disorders that frequently lead to cataract development include hypocalcemia, galactosemia, and hypoglycemia.

 

Systemic Conditions Associated with Cataracts

Cataracts located in the posterior part of the lens (posterior subcapsular cataracts) develop in more than one-third of patients with myotonic dystrophy. The formation of cataracts in the posterior subcapsular region is also notably facilitated by the systematic intake of corticosteroids. Furthermore, the following diseases or syndromes can lead to cataract development:

• Chromosomal Abnormalities: Down syndrome (Trisomy 21), Alport syndrome, Cri-du-chat syndrome ("screaming cat syndrome"), Conradi-Hünermann syndrome, Crouzon syndrome, Turner syndrome.
• Metabolic Diseases or Alimentary Disorders: Aminoaciduria (e.g., Lowe's syndrome), Fabry's disease, hypervitaminosis D, hypoparathyroidism, hypothyroidism, mucopolysaccharidoses, Wilson's disease.
• Infectious Diseases (Acquired): Cysticercosis, leprosy, onchocerciasis, and toxoplasmosis can cause secondary cataracts due to intraocular inflammation.
• Medications (as previously mentioned): Corticosteroids, haloperidol, and miotics (long-term use).

 

Visual Disturbances and Treatment of Cataracts

Visual disturbances caused by cataracts include:

• Blurred or hazy vision.
• Glare and halos around lights, especially at night.
• Reduced color perception (colors may appear faded).
• Difficulty with night vision.
• Monocular diplopia (double vision in one eye).
• Frequent changes in eyeglass prescription.
• A progressive decrease in visual acuity, while light perception is usually preserved until very advanced stages.

The only effective treatment for visually significant cataracts is surgical removal of the cataractous lens and replacement with an artificial intraocular lens (IOL). Modern cataract surgery (e.g., phacoemulsification) is a highly successful procedure that can lead to complete restoration of the patient's vision, provided there are no other coexisting eye pathologies.

 

Lens Dislocation (Ectopia Lentis)

Dislocation (luxation) or subluxation (partial dislocation) of the crystalline lens from its normal position, known as ectopia lentis, can occur with certain systemic connective tissue disorders, most notably Marfan syndrome and homocystinuria. Traumatic injury can also cause lens dislocation. A displaced lens can lead to severe visual disturbances, monocular diplopia, and can accelerate the development of secondary glaucoma (e.g., by pupillary block or angle crowding).

 

The Vitreous Body: Degeneration and Pathologies

The vitreous body (or vitreous humor) is the clear, gel-like substance that fills the large posterior cavity of the eyeball, between the lens and the retina. It helps maintain the eye's shape and transparency. With aging, the vitreous undergoes significant physical and biochemical changes (syneresis and liquefaction), similar to the aging process in other connective tissues of the body. These changes can lead to various pathologies.

 

Benign Floating Opacities ("Floaters")

Among opacities of the vitreous body, benign "floating opacities" or floaters are most commonly found. These are described by patients as small gray or white spots, strands, cobwebs, or elongated irregular objects that appear to drift or move when the eyeballs move. They are often due to age-related vitreous syneresis and liquefaction, leading to condensation of collagen fibers, or posterior vitreous detachment (PVD), where the vitreous gel pulls away from the retina.

 

Vitreous Hemorrhage

Hemorrhage into the vitreous body usually occurs from rupture of retinal blood vessels and can spread diffusely throughout the vitreous cavity, or remain localized. In cases of massive hemorrhages, vision can deteriorate significantly, sometimes to the level of light perception only. Bleeding into the vitreous body and subsequent fibrovascular membrane formation are observed in various conditions:

• Proliferative diabetic retinopathy (most common cause).
• Retinal vein occlusions (especially ischemic CRVO or BRVO with neovascularization).
• Sickle cell retinopathy (with neovascularization).
• Retinal tears or detachment.
• Trauma (blunt or penetrating).
• Age-related macular degeneration (wet AMD with subretinal hemorrhage breaking into vitreous).
• Macroaneurysms.
• Rarely, with subarachnoid hemorrhage (Terson's syndrome) due to increased intracranial pressure causing retinal/vitreous bleeding, or with traumatic brain injury.
• Malignant melanoma of the choroid or other intraocular tumors.
• Congenital anomalies of retinal vessels.

 

Asteroid Hyalosis and Other Opacities

• Asteroid Hyalosis (Benson's Disease): Characterized by the formation of numerous minute, refractile, yellowish-white spherical opacities suspended within the vitreous gel. These opacities are composed of calcium soaps (palmitate and stearate). While visually impressive on ophthalmoscopy, they usually cause minimal or no visual symptoms. This condition, reflecting a form of vitreous dystrophy, can occur in patients with diabetes mellitus, hypercholesterolemia, or often in individuals without any obvious systemic or eye disease.
• Synchysis Scintillans: Cholesterol crystals in a liquefied vitreous, often seen after chronic inflammation or hemorrhage; these tend to settle inferiorly and shower upwards with eye movement.
• Primary Amyloidosis: Vitreous opacification due to amyloid deposits can occur.
• Inflammatory Cells/Debris (Vitreitis): In uveitis or endophthalmitis.
• Tumor Cells: With certain intraocular malignancies like reticulosarcoma (primary vitreoretinal lymphoma) or retinoblastoma, tumor cells can be found floating freely in the liquid part of the vitreous or forming vitreous seeds.

 

Treatment for Vitreous Lesions (Vitrectomy)

Vitrectomy, a surgical procedure involving the removal of the vitreous gel, represents the most important advance in the treatment of many vitreous lesions. It is used to:

• Clear the vitreous from opacities like non-clearing vitreous hemorrhage or significant inflammatory debris.
• Relieve or prevent vitreoretinal traction (e.g., in tractional retinal detachment, epiretinal membranes).
• Repair retinal detachments or macular holes.
• Obtain vitreous biopsies if amyloidosis, infection, or malignancy (e.g., reticulosarcoma) is suspected; routine vitreous biopsy can provide valuable diagnostic information in such cases.

 

The Choroid: Vascular Layer and its Pathologies

The choroid is the highly vascularized layer of the eye situated between the sclera (outer white layer) and the retina. It provides nourishment to the outer retinal layers, including the photoreceptors. Lesions of the choroid itself are relatively rare in general clinical practice but can be significant.

Pathologies include:

• Choroidal Nevi: Benign pigmented lesions, common and usually asymptomatic. Require monitoring for rare malignant transformation.
• Choroidal Melanoma: The most common primary intraocular malignancy in adults. Can cause visual symptoms if large or near the macula, or lead to retinal detachment.
• Choroidal Metastases: Spread of cancer from other parts of the body (e.g., lung, breast) to the choroid.
• Choroiditis: Inflammation of the choroid, often as part of posterior uveitis or panuveitis (e.g., due to toxoplasmosis, tuberculosis, sarcoidosis).
• Choroidal Detachment: Separation of the choroid from the sclera, often due to hypotony (low intraocular pressure) after surgery or trauma, or due to fluid accumulation.
• Choroidal Hemorrhage: Bleeding within or beneath the choroid.
• Choroidal Neovascularization (CNV): Abnormal new blood vessel growth from the choroid, a key feature in wet AMD and other conditions like high myopia or angioid streaks.

Visualization of the choroid and its vessels is often enhanced by specialized imaging techniques such as indocyanine green angiography (ICGA), which is better than fluorescein angiography for imaging deeper choroidal circulation. Contrast-enhanced imaging can improve visualization of choroidal structures.

 

Diagnosis of Eye Structure Abnormalities and Visual Disturbances

A comprehensive diagnostic approach is essential for evaluating visual disturbances and pathologies of various eye structures. This includes:

1. Detailed Patient History: Onset, duration, nature of visual symptoms, associated eye or systemic symptoms, medical history, medications, family history of eye diseases.
2. Visual Acuity Testing: For distance and near vision.
3. Pupil Examination: Assessing size, shape, symmetry, and reactivity to light and accommodation.
4. Extraocular Motility Assessment.
5. Confrontation Visual Field Testing.
6. Slit-Lamp Biomicroscopy: For detailed examination of the anterior segment (cornea, anterior chamber, iris, lens) and, with special lenses (e.g., 90D, 78D, Goldmann three-mirror lens), the posterior segment (vitreous, retina, optic disc, macula).
7. Tonometry: Measurement of intraocular pressure.
8. Gonioscopy: Examination of the anterior chamber angle, crucial for glaucoma diagnosis.
9. Dilated Fundus Examination (Ophthalmoscopy): Direct visualization of the retina, optic disc, macula, and retinal vasculature after pupil dilation.
10. Specialized Imaging:
    • Optical Coherence Tomography (OCT): High-resolution cross-sectional imaging of the retina, macula, and optic nerve head.
    • Fundus Photography and Autofluorescence.
    • Fluorescein Angiography (FA) and Indocyanine Green Angiography (ICGA).
    • B-scan Ultrasonography: For imaging intraocular structures when media opacities (e.g., dense cataract, vitreous hemorrhage) prevent direct visualization.
    • Corneal Topography and Pachymetry: For corneal assessments.
11. Perimetry (Formal Visual Field Testing): To map out any visual field defects.
12. Electrophysiology (ERG, VEP, EOG): To assess retinal and optic nerve function objectively.
13. Systemic Workup: Blood tests, imaging, or consultations with other specialists (e.g., rheumatologist, endocrinologist, neurologist) if a systemic cause is suspected.

 

Differential Diagnosis of Common Visual Disturbances

Visual disturbances can arise from issues in any part of the eye or visual pathway. A few examples:

Symptom/Sign	Potential Involved Structures / Conditions
Blurred Vision	Refractive error, Cataract, Corneal opacity (keratitis, edema, scar), Macular disease (AMD, DME, macular hole), Vitreous hemorrhage/opacity, Optic neuropathy, Uveitis.
Eye Pain	Corneal abrasion/ulcer/foreign body, Acute angle-closure glaucoma, Uveitis/Iritis, Scleritis/Episcleritis, Optic neuritis (pain with eye movement), Orbital cellulitis.
Red Eye	Conjunctivitis (viral, bacterial, allergic), Keratitis, Uveitis, Acute angle-closure glaucoma, Scleritis/Episcleritis, Subconjunctival hemorrhage.
Floaters and Flashes	Posterior vitreous detachment (PVD), Retinal tear or detachment, Vitreous hemorrhage, Uveitis (inflammatory cells), Migraine aura.
Peripheral Vision Loss	Glaucoma, Retinal detachment, Retinitis pigmentosa, Optic neuropathy, Stroke affecting visual pathway, Chiasmal lesions.
Central Vision Loss/Distortion	Macular degeneration (AMD), Diabetic macular edema, Macular hole, Epiretinal membrane, Central serous chorioretinopathy, Optic neuropathy affecting central fibers.

 

Prevention and When to Consult an Ophthalmologist

Preventive measures include regular comprehensive eye exams (especially with age or risk factors), controlling systemic diseases (diabetes, hypertension), UV protection, eye safety during hazardous activities, and maintaining a healthy lifestyle. Consult an ophthalmologist promptly for:

• Sudden changes in vision (loss, blurriness, distortion).
• Sudden onset of severe eye pain or redness.
• New onset of flashes of light or a shower of floaters.
• A "curtain" or "shadow" obscuring part of your vision.
• Suspected eye injury or foreign body.
• Gradual but progressive worsening of vision.
• Persistent eye discomfort, dryness, or irritation.

Early detection and treatment of eye diseases are crucial for preserving vision.