Introduction to Ophthalmology Ophthalmology 160.01

Fall 2019 Tuesdays 12:10-1 pm Location: Library, Room CL220&223

University of California, San Francisco WELCOME

OBJECTIVES This is a 1-unit elective designed to provide 1st and 2nd year medical students with - General understanding of anatomy - Knowledge of the basic components of the eye exam - Recognition of various pathological processes that impact vision - Appreciation of the clinical and surgical duties of an ophthalmologist

INFORMATION This elective is composed of 11 lunchtime didactic sessions. There is no required reading, but in this packet you will find some background information on topics covered in the lectures. You also have access to Vaughan & Asbury's General Ophthalmology online through the UCSF library.

AGENDA 9/10 Introduction to Ophthalmology Neeti Parikh, MD CL220&223 9/17 Oculoplastics Robert Kersten, MD CL220&223 9/24 Ocular Effects of Systemic Processes Gerami Seitzman, MD CL220&223 10/01 Refractive Surgery Stephen McLeod, MD CL220&223 10/08 Comprehensive Ophthalmology Saras Ramanathan, MD CL220&223 10/15 BREAK- AAO 10/22 The Role of the Microbiome in Bryan Winn, MD CL220&223 10/29 Retinal imaging in patients with hereditary retinal degenerations Jacque Duncan, MD CL220&223 11/05 Pediatric Ophthalmology Maanasa Indaram, MD CL220&223 11/12 Understanding from a Circuit Perspective Yvonne Ou, MD CL220&223 11/19 11/26 Break - Thanksgiving 12/03 Retina/Innovation/Research Daniel Schwartz, MD CL220&223

CONTACT Course Director Course Coordinator Dr. Neeti Parikh Shelle Libberton [email protected] [email protected] ATTENDANCE Two absences are permitted. Please let Shelle Libberton know if you are planning to be absent or have missed a class.

See the UCSF Vision and Ophthalmology Interest Group website for more information:

Please feel free to contact the coordinator first with any questions or concerns. **don’t forget to officially sign up for the class** https://sites.google.com/site/ucsfpreophthalmology/

Eye Anatomy & Physiology

When looking into someone's , we can easily see several structures: - A black-looking aperture, the , that allows light to enter the eye. - A colored circular muscle, the , which controls the size of the pupil so that more or less light, depending on conditions, is allowed to enter the eye - A transparent external surface, the , that covers both the pupil and the iris. This is the first and most powerful of the optical system of the eye and allows, together with the crystalline lens the production of a sharp image at the retina. - The "white of the eye", the , which forms part of the supporting wall of the eyeball is continuous with the cornea and the dura of the central nervous system.

The eye has three chambers of fluid: Anterior chamber (between cornea and iris), Posterior chamber (between iris, zonule fibers and lens) and the (between the lens and the retina). The first two chambers are filled with aqueous humor whereas the vitreous chamber is filled with a more viscous fluid, the vitreous humor.

The sagittal section of the eye also reveals the lens which is a transparent body located behind the iris. The lens is suspended by ligaments (called zonule fibers) attached to the anterior portion of the . The contraction or relaxation of these ligaments as a consequence of actions, changes the shape of the lens, a process called that allows us to form a sharp image on the retina.

Light rays are focussed through the transparent cornea and lens upon the retina. The central point for image focus (the visual axis) in the human retina is the fovea. Here a maximally focussed image initiates resolution of the finest detail and direct transmission of that detail to the brain for the higher operations needed for perception. Slightly more nasally than the visual axis is the optic axis projecting closer to the optic nerve head. The optic axis is the longest sagittal distance between the front or vertex of the corna and the furthest posterior part of the eyeball. It is about the optic axis that the eye is rotated by the eye muscles.

Inserted into the sclera are three pairs of muscles (6 muscles altogether). Two pairs are rectus muscles running straight to the bony of the skull orthogonal to each other (the superior rectus, the inferior rectus, the lateral rectus and the medial rectus muscles). A further pair of muscles, the oblique muscles (superior oblique and inferior oblique) are angled as the name implies obliquely. These muscles, named extraocular muscles rotate the eyeball in the orbits and allow the image to be focussed at all times on the fovea of central retina.

The retina is a part of the central nervous system and an ideal region of the vertebrate brain to study, because like other regions of the central nervous system, it derives from the neural tube. The retina is formed during development of the embryo from optic vesicles outpouching from two sides of the developing neural tube. The primordial optic vesicles fold back in upon themselves to form the with the inside of the cup becoming the retina and the outside remaining a single monolayer of epithelium known as the retinal pigment epithelium. Initially both walls of the optic cup are one cell thick, but the cells of the inner wall divide to form a neuroepithelial layer many cells thick: the retina

In the center of the retina is the optic nerve, a circular to oval white area measuring about 2 x 1.5 mm across. From the center of the optic nerve radiate the major blood vessels of the retina. There are two sources of blood supply to the mammalian retina: the central retinal artery and the choroidal blood vessels. The receives the greatest blood flow (65-85%) (Henkind et al., 1979) and is vital for the maintainance of the outer retina (particularly the photoreceptors) and the remaining 20-30% flows to the retina through the central retinal artery from the optic nerve head to nourish the inner retinal layers. The central retinal artery has 4 main branches in the human retina.

The arterial intraretinal branches then supply three layers of capillary networks i.e. 1) the radial peripapillary capillaries (RPCs) and 2) an inner and 3) an outer layer of capillaries. The precapillary venules drain into venules and through the corresponding venous system to the central retinal vein.

Approximately 17 degrees (4.5-5 mm), or two and half disc diameters to the left of the disc, can be seen the slightly oval- shaped, blood vessel-free reddish spot, the fovea, which is at the center of the area known as the macula by ophthalmologists.

A circular field of approximately 6 mm around the fovea is considered the central retina while beyond this is peripheral retina stretching to the , 21 mm from the center of the . The total retina is a circular disc of approximately 42 mm diameter.

The retina is approximately 0.5 mm thick and lines the back of the eye. The optic nerve contains the ganglion cell axons running to the brain and, additionally, incoming blood vessels that open into the retina to vascularize the retinal layers and neurons. A radial section of a portion of the retina reveals that the ganglion cells (the output neurons of the retina) lie innermost in the retina closest to the lens and front of the eye, and the photosensors (the rods and cones) lie outermost in the retina against the pigment epithelium and choroid. Light must, therefore, travel through the thickness of the retina before striking and activating the rods and cones. Subsequently the absorbtion of photons by the visual pigment of the photoreceptors is translated into first a biochemical message and then an electrical message that can stimulate all the succeeding neurons of the retina. The retinal message concerning the photic input and some preliminary organization of the visual image into several forms of sensation are transmitted to the brain from the spiking discharge pattern of the ganglion cells.

A simplistic wiring diagram of the retina emphasizes only the sensory photoreceptors and the ganglion cells with a few interneurons connecting the two cell types such as seen in the figure 2.

References: Kolb, H., Fernandez, E., & Nelson, R. (2003) Webvision: Organization of the Retina and . Retrieved April 15, 2007 from http://webvision.med.utah.edu/. “Red Eye”

Differential diagnosis: • Conjunctivitis (viral, bacterial, allergic): most common; dilatation of superficial conjunctival blood vessels resulting in hyperemia, edema, and discharge. • Uveitis: inflammation of the iris and ciliary body, usually in young or middle-aged patients; its hallmark is the presence of inflammatory cells and protinaceous flare in the anterior chamber of the eye • Acute angle-closure glaucoma: a narrow anterior chamber angle can occur in patients with hyperopia (farsightedness) and older patients resulting in rapid elevation of intraocular pressure • Keratitis (corneal ulcer or inflammation, eg, herpes simplex): inflammation of the and superficial stroma; present in cases of corneal abrasion or contact lens overwear • Scleritis: can impair vision and may be associated with vascular or connective tissue disease; prompt treatment needed • Episcleritis: self-limited, recurrent, presumably autoimmune inflammation of the episcleral vessels • Subconjunctival hemorrhage: redness is unilateral and well-circumscribed; underlying sclera is not visible and adjacent sclera is free of inflammation; may be due to trauma, anticoagulation, hypertension, excessive coughing or vomiting • disorder (eg, blepharitis): inflammation of the eyelid often associated with conjunctival inflammation, caused by a variety of infectious agents, allergic disorders, and dermatologic diseases

Patient evaluation: The following are important questions to ask while taking the patient history: • Is vision affected? • Is there foreign body sensation? May suggest corneal involvement. • Is there photophobia? • Was there trauma? • Is the patient a contact lens wearer? May suggest keratitis. • Is there discharge, other than tears, that continues throughout the day? May suggest conjunctivitis or keratitis. On penlight examination: • Does the pupil react to light? Fixed pupil in angle closure glaucoma. • Is the pupil very small (1-2 mm) in size? Suggests corneal abrasion, infectious keratitis, iritis. • What is the pattern of redness? • Is there a white spot, opacity or foreign body on the cornea? Suggests infectious keratitis. • Is there hypopyon (a layer of white cells in the anterior compartment)? Suggests infectious keratitis. Is there hyphema (layer of red cells)? Suggests trauma.

The table above was taken from Leibowitz, HM. The red eye. N Engl J Med 2000; 343:345. References: (1) Differential Diagnosis: Red eye. Access Medicine. Retrieved 15 April 2007 from AccessMedicine. http://www.accessmedicine.com/diag.aspx?code=114382. (2) Leibowitz, HM. The red eye. N Engl J Med 2000; 343:345. (3) Evaluation of the red eye. Up to date online. Retrieved 15 April 2007 from http://www.utdol.com/utd/content/topic.do?topicKey=priophth/4412&type=A&selectedTitle=1~11 Macular Degeneration & Neuroophthalmology

Age-related macular degeneration (AMD) is a disease of the eye that is the leading cause of blindness for people aged 65 years and older and affects more than 10 million Americans. AMD is caused by a deterioration of the macula, the center of the retina that is responsible for the detailed central vision that allows people to read, drive, and recognize faces.

Risk factors for AMD include older age, white race, and smoking. There is no cure for AMD, but therapies are available that can slow the disease.

There are two different forms of AMD: In atrophic AMD (dry form), there is irregular pigmentation of the macular region but no elevated macular scar and no hemorrhage or exudation in the macular region. In exudative AMD (wet or neovascular form), which is much less common, a subretinal network of choroidal neovascularization forms. This network is often associated with hyperpigmentation of the macula and soft drusen (small yellow deposits that form under the macula). A localized elevation of an area of the macula or a pigment epithelial detachment may be caused by hemorrhage or fluid accumulation. Eventually, this network leaves an elevated scar at the posterior pole.

Ninety percent of the blindness caused by AMD occurs in the 10% of cases that have the exudative form.

Symptoms, Signs, and Diagnosis Both forms of AMD are often bilateral and are preceded by development of drusen. In atrophic AMD, central visual acuity is lost slowly and painlessly. Rapid vision loss is more typical of exudative AMD. Although peripheral vision and color vision are generally unaffected, the patient may become legally blind (< 20/200 vision) in the affected eye(s). The first symptom of exudative AMD is visual distortion in one eye, which can be detected with an Amsler grid (see left).

Central blind spots (scotomas) usually develop early in atrophic AMD. Funduscopy reveals pigmentary or hemorrhagic disturbance in the macular region of the involved eye; the contralateral eye almost always shows some pigmentary disturbance and drusen in the macula. Other findings may include retinal detachment, lipid exudates, tissue atrophy, and macular scarring.

AMD is diagnosed by clinical appearance of the retina. Fluorescein angiography may reveal a neovascular membrane beneath the retina. An angiogram is obtained when findings suggestive of neovascularization are present; such findings include subretinal hemorrhage, localized retinal elevation, retinal edema, and gray discoloration of the subretinal space. Fluorescein angiography demonstrates and characterizes a subretinal choroidal neovascular membrane.

Prognosis and Treatment Atrophic AMD produces mild to moderate reduction of vision but rarely leads to blindness. There is no recommended treatment, but patients at risk of advanced disease (eg, those with large drusen or irregular macular pigmentation) may benefit from daily supplements of zinc oxide with copper, vitamin C, vitamin E, and beta carotene.

If exudative AMD is untreated, vision typically deteriorates substantially, often to blindness. However, peripheral vision is usually retained. Results of treatment depend on the size, location, and type of neovascularization. Thermal laser photocoagulation of neovascularization outside the fovea may prevent severe vision loss. Photodynamic therapy, a laser treatment, provides benefit under specific circumstances. Pegaptanib is a new injectable selective vascular endothelial growth factor antagonist that can be used for the treatment of neovascular AMD.

For patients who have lost central vision, low-vision devices, such as magnifiers, high-power reading glasses, computer monitors, and telescopic lenses, are available. Low-vision counseling is advised.

References: Parmet, S. (2006) Age-Related Macular Degeneration. JAMA. 295:2438. “Age-Related Macular Degeneration.” (2006) The Merck Manual of Diagnosis and Therapy, 18th ed. Neuroophthalmology is an ophthalmic subspecialty that addresses the relationship between the eye and the brain, specifically disorders of the optic nerve, orbit, and brain, associated with visual symptoms. Symptoms that are more common in neuro- ophthalmic disease include visual loss, visual disturbance, diplopia (double vision), unequal , and eyelid and facial spasms. A partial list of the most common neuro-ophthalmic conditions is listed below with select details: • optic neuritis: inflammation of the optic nerve. Symptoms are usually unilateral, with eye pain and partial or complete vision loss. Diagnosis is primarily clinical. Treatment is directed at the underlying condition; most cases resolve spontaneously. o Optic neuritis is most common in adults 20 to 40 yr. Most cases result from demyelinating disease, particularly multiple sclerosis, in which case there may be recurrences. Other causes include infectious disease, tumor metastasis to the optic nerve, chemicals and drugs, and, rarely, diabetes, pernicious anemia, Graves' disease, bee stings, and trauma. Often, the cause remains obscure despite thorough evaluation. • ischemic optic neuropathy (including temporal arteritis): infarction of the optic disk. The only symptom is painless vision loss. Diagnosis is clinical. Treatment is ineffective. o Most ischemic optic neuropathy is unilateral. Bilateral, sequential cases occur in about 20%, but bilateral simultaneous involvement is uncommon. Two varieties of optic nerve infarction exist, nonarteritic (more frequent, typically people 50-70 yr) and arteritic (less frequent, more severe, patients typically >70 yr). Atherosclerotic narrowing of the posterior ciliary arteries may predispose to nonarteritic optic nerve infarction, particularly after a hypotensive episode. Any of the inflammatory arteritides, especially temporal arteritis, can precipitate the arteritic form. Diagnosis of the arteritic form is important, not because anything can be done to improve the involved eye, but rather to begin preventive treatment of the other eye. • papilledema (including pseudotumor cerebri): swelling of the optic disk due to increased intracranial pressure. All other causes of optic disk swelling, such as that due to malignant hypertension or thrombosis of the central retinal vein, do not involve increased intracranial pressure and therefore are not causes of papilledema. Papilledema requires an immediate search for the cause. There are no early symptoms, although transiently diminished vision lasting only seconds can occur. Diagnosis is by ophthalmoscopy with further tests, usually brain imaging, to determine cause. Treatment is directed at the underlying condition. o Cause can be a brain tumor or abscess, cerebral trauma or hemorrhage, meningitis, arachnoidal adhesions, cavernous or dural sinus thrombosis, or encephalitis. Papilledema also occurs with idiopathic intracranial hypertension (pseudotumor cerebri), a condition with elevated CSF pressure and no mass lesion. • hereditary optic neuropathies: genetic defects that cause vision loss, occasionally with cardiac or neurologic abnormalities. They typically present in childhood or adolescence with bilateral, central vision loss. There is no effective treatment. o Dominant optic atrophy is inherited in an autosomal dominant fashion. It is believed to be the most common of the hereditary optic neuropathies, with prevalence in the range of 1:10,000 to 1:50,000. o Leber's hereditary optic neuropathy has a mitochondrial DNA abnormality that affects cellular respiration. Males are affected 80 to 90% of the time. • compressive optic neuropathy (including pituitary tumors) • cerebrovascular disorder involving vision • tumors involving vision • blephrospasm (including botulinum injections) • hemifacial spasm (including botulinum injections) • thyroid eye disease • myasthenia gravis • ocular motor disorders (including cranial nerve palsies) • pupillary abnormalities • paraneoplastic disorders (including paraneoplastic retinopathies and optic neuropathies)

Resources: “Eye Care: Neuro-Ophthalmology.” Bascom Palmer Eye Institute. Retrieved on April 15. 2007 from http://www.bpei.med.miami.edu/site/disease/disease_neuro.a sp. “Ocular Nerve Disorders.” (2006) The Merck Manual of Diagnosis and Therapy, 18th ed. Ocular Trauma

INTRODUCTION:

Ocular trauma can result in loss of vision and disability. Types of ocular trauma include closed and open injury, rupture, laceration, penetrating injury, intraocular foreign body injury, and perforating injury and chemical burns.

CLASSIFICATIONS: Definitions of the proposed ocular traumatology terms

Term Definition Remarks Eye Wall Sclera and cornea Though technically the wall of the eye has not one but three tunics (coats) posterior to the limbus, for clinical purposes it is best to restrict the term “eyewall” to the rigid structures of the sclera and cornea Either there is no corneal or scleral wound at all (contusion) Closed globe The eye wall does not have a or it is only of partial thickness (lamellar laceration). Rarely, injury full-thickness wound a contusion and a lamellar laceration may coexist

Open globe injury The eye wall has a full- The cornea and/or the sclera sustain a through-through thickness wound injury. Depending on the inciting object’s characteristics and the injury’s circumstances, ruptures and lacerations are distinguished. The and the retina may be intact, prolapsed, or damaged. The eye is a ball filled with incompressible liquid. A blunt Rupture Full-thickness wound of the object with sufficient momentum creates energy transfer eye wall, caused by a blunt over a large surface area, greatly increasing the IOP. The object. The impact results in eye wall gives way at its weakest point which may or may momentary increase of the not be at the impact site. The actual wound is produced by Intraocular pressure (IOP) and an inside-out force; consequently, tissue herniation is very an insidious injury mechanism. frequent and can be substantial. Further classification is based on whether an exit wound or an intraocular foreign body (IOFB) is also present. Laceration Full-thickness wound of the Occasionally, an object may create a posterior (exit) wound eye wall, usually caused by a while remaining, at least partially, intraocular. sharp object. The wound occurs at the impact site by an outside-in mechanism. Single laceration of the eye Penetrating wall, usually caused by a sharp No exit wound has occurred. If more than one entrance object wound is present, each must have been caused by a Retained foreign object(s) different agent. An IOFB injury is technically a penetrating injury but is Intraocular foreign causing entrance laceration(s) grouped separately because of different clinical implications body injury (treatment modality, timing, rate of endophthalmitis, etc. The two wounds must have been caused by the same agent. Perforating injury Two full-thickness lacerations (entrance and exit) of the eye wall, usually caused by a sharp object or missile Alkaline and Acidic Chemical Burns Exposure to alkaline chemicals (drain cleaners, chemical detergents, industrial solvents) can produce liquefactive necrosis that dissolves tissue. Alkali damage can only be interrupted by treatment/removal of the offending agent. Acid burns are often less severe than alkali burns. Acid results in coagulation necrosis and the precipitation of proteins on the surface of the eye. These proteins limit the depth of injury.

The above is from Kuhn F, et al: A standardized classification of ocular trauma and Douglas D. Brunette, Chapter 70 – Ophthalmology, In Marx: Rosen's Emergency Medicine. EVALUATION: An initial ophthalmic evaluation includes differentiation between penetrating and non-penetrating injury as well as an evaluation of the extent of injury and associated extraocular trauma. The patient’s history may provide clues to the nature of the trauma and any associated injuries. Advances in medical and surgical management including modern diagnostic techniques, surgery and rehabilitation can aid in the treatment of ocular trauma and prevention of vision loss.

REFERENCES:

Aaberg TM, Capone Jr A, de Juan Jr E, et al: A system for classifying mechanical injuries of the eye. Am J Ophthalmol 1997; 123:820-831.

Babar TF, Khan MT, Marwat MZ, et al: Patterns of ocular trauma. J Coll Physicians Surg Pak. 2007 Mar;17(3):148-53.

Douglas D. Brunette, Chapter 70 – Ophthalmology, In Marx: Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed. Mosby, Inc. Retrieved 04, 15, 2007, from Elsevier.

Kuhn F, Morris R, Witherspoon D, et al: A standardized classification of ocular trauma. Ophthalmology 1996; 103:240-243. Cataract & Glaucoma

Cataract is the leading cause of blindness in the world. According to the World Health Organization, they affect an estimated 20 million people worldwide. A cataract is a cloudy or opaque region of the normally transparent lens in the eye, often resulting in blurry vision, poor , or sensitivity to light.

The lens is located behind the colored part of the eye, which is called the iris. It consists of three parts: the capsule, the cortex and the nucleus. The capsule is the outer membrane that surrounds the cortex, which then surrounds the center of the lens--its nucleus.

Just like there are three regions of the lens, there are three types of cataracts. The most common clouding of the lens occurs in the nucleus. Typically this nuclear cataract is found in older people. The lens gradually grows cloudy as the person ages. When the opaque area increases, it prevents light rays from passing through the lens to focus on the retina, the light sensitive tissue at the back of the eye. Typically the person experiences blurred vision, glare, increased nearsightedness, and distortion of images that they see in either eye. The longer we live, the more likely we are to develop cataracts. Over 60% of people whose visual acuity is less than 20/400 (WHO definition of blindness) have age-related cataracts.

Healthy Eye Eye with a Cataract There is also a cortical cataract that affects the lens cortex. These opacities originate on the outside edges of the lens and seem like wedge-shaped spokes of a bicycle. When they gradually extend toward the center of the lens, they interfere with the path of light and significantly affect both near and distance vision. People who have diabetes tend to develop these types of cataracts.

Finally, subcapsular cataracts start to develop as small opacities at the back of the lens. They are also associated with diabetes. They start to affect vision when they have grown quite significantly. Sometimes when people have to use drops like corticosteroids in their eyes to treat inflammation, the active ingredients in these drops can cause the proteins to become cloudy.

Although age is a significant factor, they are also caused by injuries like inadvertently hitting the eye. Someone can be born with cataracts or acquire them when they are exposed to damaging sunrays or certain chemicals.

Traumatic cataracts are caused by being hit in the eye. In those cases, the cataract forms in the back of the cortex and leads to progressive loss of vision. When a sharp object punctures the eye and comes in contact with the lens capsule, the lens totally opacifies either immediately or at some later time.

Babies born with cataracts have what is called congenital cataracts. They occur most often when the mom has some sort of infection, like rubella, or sometimes other family members also have cataracts and the baby gets them because of a genetic link.

The environment plays a key role in cataract formation. The lens is made up of protein, a substance that is configured in a way to be completely clear. It's necessary for this protein to be clear in order for us to see through it. Sun emits ultraviolet rays that cause the lens protein to stop being clear. Some chemicals in the environment may be able to reach through the outer layers of the eye and can affect those lens proteins, also causing them to become opaque. These types of cataracts are called "induced" cataracts.

The most effective and common treatment is to surgically remove the cloudy lens. There are two types of cataract surgery: 1. Phacoemulsification, or phaco. A small incision is made on the side of the cornea, the clear, dome-shaped surface that covers the front of the eye. A tiny probe is inserted into the eye. This device emits ultrasound waves that soften and break up the lens so that it can be removed by suction. Most cataract surgery today is done by phacoemulsification, also called "small incision cataract surgery." 2. Extracapsular surgery. A longer incision is made on the side of the cornea and removes the cloudy core of the lens in one piece. The rest of the lens is removed by suction. After the natural lens has been removed, it often is replaced by an artificial lens, called an intraocular lens (IOL). An IOL is a clear, plastic lens that requires no care and becomes a permanent part of the eye. Light is focused clearly by the IOL onto the retina, improving vision. Some people cannot have an IOL. They may have another eye disease or have problems during surgery. For these patients, a soft contact lens, or glasses that provide high magnification, may be suggested.

References: National Eye Institute Eye Information: Cataract (http://www.nei.nih.gov/health/cataract/cataract_facts.asp) Unite For Sight Online Eye Health Course (http://www.uniteforsight.org/course/cataracts.php)

Glaucoma is a condition resulting from too much aqueous humor present in the eye, causing the pressure to rise and push against the optic nerve, resulting in nerve damage and vision loss. It is caused by damage to the eye's optic nerve. If detected and treated early, permanent damage can be minimized or even avoided. Once damages occurs, however, it cannot be reversed.

There are many types of glaucoma. The most common form is open angle glaucoma, also called chronic glaucoma. Open angle glaucoma is caused by high pressure in the eye, which damages the optical nerve and impairs vision. Increased eye pressure does not always mean you will get glaucoma, but it does increase your risk. Another type of glaucoma is low-tension or normal tension glaucoma, which occurs when the optic nerve is damaged despite seemingly normal pressure levels. Treatment is the same as open angle glaucoma. Closed-angle glaucoma is also common, caused when the iris and lens essentially stick together, preventing fluid flow from the eye. Glaucoma can also occur as a result of an injury such as being hit in the eye by a baseball. This is called secondary glaucoma.

Symptoms At first, open-angle glaucoma has no symptoms. It causes no pain, and vision stays normal.

If glaucoma is untreated, vision slowly worsens. Peripheral vision (to the sides) is usually the first to deteriorate.

If glaucoma remains untreated, people may miss objects to the side and out of the corner of their eye.

If treatment is not given, vision reduces until no vision remains.

Detection There are many tests that can be done by your doctor or eye care professional to detect glaucoma. Usually intraocular pressure tests and visual field tests are performed in combination to determine the eye's pressure and the pressure's affect on the optic nerve. Photographs of the optic nerve may also be taken to determine the health of the optic nerve. These simple tests can ensure that the disease is diagnosed early, so it can be treated before permanent damage is caused.

Treatment options There is no cure for glaucoma. Damage done to the optic nerve is permanent. There are, however, many treatment options that can minimize the effect and prevent further damage. Treatments include eye drops, laser trabeculoplasty, or conventional surgery. These treatments are often used together.

Medication can be used to reduce eye pressure, preventing further damage to the optic nerve. Eye drops are the most common type of medicine. Pills may also be used.

Laser trabeculoplasty is a treatment performed by a doctor or eye care professional. A laser machine is used to improve the drainage in the eye. This is a longer-term solution than medicine, but the effect will reduce over time.

In conventional surgery, a small piece of tissue is removed from the eye, which creates a new opening for the fluid to leave the eye.

Glaucoma can affect everyone. The most common groups who are affected are: Persons of African descent over the age of 40 and persons of Mexican descent Everyone over age 60 People with a family history of glaucoma.

References: Unite For Sight Online Eye Health Course (http://www.uniteforsight.org/course/glaucoma.php)