Dr Ben Wild Most of the focusing power of the eye comes from the cornea, the clear tissue in front of the colored iris, and the intra-ocular lens, a clear tissue located through the pupil. Normally, when the eye is focused on a distant target, the muscles that control the intra-ocular lens's shape are relaxed and when the eye is focused on a near target, the muscles are tensed. This change in intra-ocular lens shape is what enables the eye to see a distant target clearly and then switch to see a near target clearly. A sagittal view of light from a distant object focusing on the retina (top) and light from a near target focusing on the retina (bottom). Unfortunately, the intra-ocular lens never stops growing. Presbyopia occurs when the intra-ocular lens itself becomes sufficiently large and sufficiently stiff that the muscles that control its shape are no longer strong enough to sufficiently change its shape. This leads to the inability to focus both distant and near targets without the use of 2 different prescriptions. A sagittal view of a lens unable to focus the light from a near object on the retina. Reading glasses would be needed to focus this light back on the retina but would then also make a distant object out of focus. Presbyopia usually starts between the late 30s and mid 40s and progresses until the lens becomes completely static between the early and late 50s. It does not progress beyond this point. Signs Inability to see up close when the eyes are properly corrected for distance, squinting. Symptoms Eyestrain, headaches, difficulty switching between distance and near targets. Causes The intra-ocular lens grows sufficiently large and becomes sufficiently hard that it can no longer change shape. Changing shape is needed for changing focus. Risk Factors Age. Presbyopia occurs to everybody between late 30s and mid 40s. Prevention There are no known preventative measures. Treatments · Reading glasses. · Bifocal or trifocal glasses. · Progressive glasses. · Monovision laser surgery, lens replacement surgery or contact lenses. · Multifocal lens replacement surgery or contact lenses. · Pilocarpine eye drops. Presbyopia occurs in everybody. It is not a disease and does not increase risk of developing any eye disease. It is a normal part of ageing.

Dr Ben Wild As our bodies develop from birth until adulthood, our eyes have to change in lock-step. This process is called emmetropization (where the growth of the eye matches the change in focusing power). Most of the focusing power of the eye comes from the cornea, the clear tissue in front of the colored iris, and the intra-ocular lens, a clear tissue located through the pupil. A sagittal view of an eye with light rays focusing perfectly on the retina. Hyperopia, or farsightedness, is usually present at birth and unlike myopia, does not usually progress over time. Hyperopia occurs when the cornea and the lens focus light behind the retina (the back surface of the inside of the eye responsible for sensing light). When young, the intra-ocular lens is able to change shape to allow the light from both distant and near objects to be focused on the retina. The patient may experience symptoms like eye strain after prolonged near work or may be asymptomatic with mild hyperopia. Moderate to high hyperopia is usually symptomatic. As the eye ages, around late 30s or early 40s, the intra-ocular lens loses the ability to change shape and both distance and near vision become blurry. A sagittal view of a hyperopic eye with light rays focusing behind the retina (top) and a view of a hyperopic eye with glasses that are helping focus the light on the retina (bottom). Signs Often no signs, possibly esotropia (crossed eye). Symptoms Eyestrain, headaches, difficulty changing focus from far to near and/or vice versa. Causes Small eye or the focusing power of the cornea and lens is too weak. Risk Factors Genetics. Prevention There are no preventative measures. Treatments · Glasses. · Contact lenses (soft, hard, and orthokeratology). · Laser eye surgery. Hyperopia does not lead to any eye diseases like myopia. However, smaller eye sizes can increase the risk of angle closure glaucoma. High levels of hyperopia can cause a an eye turn (inwards) around the age of 2-3 years old that can be corrected just with glasses.

Dr Ben Wild As our bodies develop from birth until adulthood, our eyes have to change in lock-step. This process is called emmetropization (where the growth of the eye matches the change in focusing power). Most of the focusing power of the eye comes from the cornea, the clear tissue in front of the colored iris, and the intra-ocular lens, a clear tissue located through the pupil. A sagittal view of an eye focusing a dot of light on the retina. Astigmatism occurs when the cornea and/or lens start to grow into the shape of a cylinder and not a sphere. This means that the eye requires a corrective lens that is equally shaped as a cylinder but pointed in the opposite direction. The technical definition of astigmatism is the inability to focus a dot of light into a dot of light. Instead, the light is focused as a line of light. A sagittal view of an eye focusing a dot of light on the retina as a line of light (top) and an eye with a cylindrical glass lens refocusing the light as a dot of light on the retina (bottom). Astigmatism isn't caused by doing anything wrong but has been associated with large amounts of reading and near work. It can sometimes be seen at birth. Signs Squinting. Symptoms Eyestrain, headaches, blurry near and distance vision, dots of light (headlights) look like lines of light. Causes Usually, astigmatism originates from the cornea developing into the shape of a cylinder instead of a sphere. Occasionally the intra-ocular lens can be in the shape of a cylinder. Risk Factors Genetics, corneal ectasia (like keratoconus), eye infections or scarring, excessive near work. Prevention There are no preventative measures. Treatments · Glasses. · Contact lenses (soft and hard). · Laser eye surgery. Astigmatism does not usually progress past teenage years and does not cause any eye disease like myopia. There are some eye conditions that can cause astigmatism, such as corneal ectasias, scarring, and more, but generally it is due to the development of the eye. Glasses, contact lenses and laser eye surgery can be very well utilized for clear vision. If high amounts of astigmatism go uncorrected for too long as a child, the visual cortex of the brain may never fully develop and vision, even with the best glasses prescription, may never reach 20/20. This is called amblyopia. It is important to correct astigmatism in youth.

Dr Ben Wild The retina is located at the back surface of the inside of the eye. Its main function is to detect and transmit the sensation of light to the brain for interpretation. Attached to the retina is the vitreous humor. The vitreous humor is a large scaffold of gel that helps keep the eye inflated and extends from the retina all the way to the lens near the front of the eye. A sagittal view of a healthy eye where the vitreous humor gel represents the pink space between the lens and the retina. A posterior vitreous detachment (PVD) refers to the separation of the vitreous humor from the retina. This is usually a normal process cause by the liquefaction and shrinking of the gel due to age but can be caused by cataract surgery, trauma, inflammation inside the eye or laser retinopexy surgery. 65% of people have had a PVD by the age of 65. The separation usually starts around the macula (the part of the retina that corresponds to the center of vision) then the peripheral retina then around the optic nerve. A sagittal view of an eye that has had a PVD. The vitreous gel is seen separated from the retina. Signs Weiss ring (large circular floater), rare retinal bleeding, rare torn blood vessels, possible pigment granules in the vitreous humor, rare torn retina. Symptoms Flashes of light like lightning bolts or arcs associated with head turn or eye movement, floaters (myodesopsia). Causes Liquefaction and shrinkage of the vitreous humor. Risk Factors Age, cataract surgery, trauma, uveitis (inflammation inside the eye), laser retinal surgery. Prevention There are no known preventative measures. Treatments · Get retinal exam within 48 hours, ideally 24 hours. · If a retinal tear is also seen, immediate laser retinopexy surgery. A PVD is a normal occurrence and usually results in a permanent floater. Often, the floater will settle downwards out of view or the brain will adapt and tune out the floater. If there is a torn blood vessel, bleeding in the vitreous humor or bleeding in the retina after a PVD, there is a high likelihood of a retinal tear. A tear can be repaired with laser retinal surgery easily without any permanent loss of vision. If not treated in time, a tear can lead to a retinal detachment and cause permanent vision loss.

Dr Ben Wild The retina is located at the back surface of the inside of the eye. Its main function is to detect and transmit the sensation of light to the brain for interpretation. Attached to the retina is the vitreous humor. The vitreous humor is a large scaffold of gel that helps keep the eye inflated and extends from the retina all the way to the lens of the eye. Sagittal view of a healthy eye. A retinal tuft is an abnormality present at birth (congenital) that is often in one of two main forms; cystic and zonular tufts. Cystic tufts are seen as elevated white bumps in the peripheral retina in 5% of people and are formed of glial cells that are strongly attached to both the retina and the vitreous gel. Zonular tufts occur when a zonule, zonules being the cables that hold the lens of the eye in place, attaches to the retina instead of the ciliary body muscle. This attachment site usually leads to traction and pulling of the retina. Zonular tufts can be seen in up to 15% of people. A sagittal view of an eye with a zonular tuft (white line extending from the lens to the retina) and a cystic tuft (white spot on retina). Signs Symptoms Asymptomatic (no symptoms). Causes Congenital abnormality. Risk Factors There are no known risk factors. Prevention There are no known preventative measures. Treatments · Close monitoring every 1-2 years for development of a retinal hole or tear. · If a retinal hole or tear occurs; laser retinopexy surgery. Cystic tufts cause 10% of all retinal detachments but the risk of a retinal detachment for a patient with a cystic tuft is under 1%. Regular eye exams can help detect any changes that may require surgery before a retinal detachment occurs. The vast majority of cases do not require any treatment and vision is never affected. Zonular tufts have a 2% lifetime risk of developing into a retinal detachment. Regular eye exams can decrease the odds of this occurring. For either tuft, seek medical attention same day with any new flashes of light, floaters or a veil appearance in vision.

Dr Ben Wild Our vision comes from light waves stimulating retinal photoreceptors and these photoreceptors transferring their signals through the several different cells in the retina and onwards to the brain. For light to focus on the retina, it must pass through the cornea (front of the eye), the pupil, then lens and the clear vitreous humor gel. Sagittal view of a healthy eye. Lattice and snail track degenerations are mostly bilateral (both eyes) conditions thought to develop early in life (2nd or 3rd decade) most commonly in people who have moderate to high nearsightedness. Simply put, they are like stretch marks on the retina. Snail tracks are white spindle shaped areas of retinal thinning. It is thought that this thinning then leads to pulling of the retina by the vitreous humor gel leading to lattice formation. Lattice presents as spindle shaped pigmented lines on the retina, often with white blood vessels overtop, often with retinal holes nearby, and liquefied vitreous gel overtop known as lacunae. Lattice degeneration is the most important degeneration linked to retinal detachments as 40% of all retinal detachments occur in eyes with lattice degeneration although only 1% of eyes with lattice degeneration develop a retinal detachment. A sagittal view of an eye with snail track degeneration (white) and lattice degeneration (black) with a retinal hole nearby. Signs Symptoms Asymptomatic (no symptoms). Causes Thin retina due to genetics or due to overgrowth of the eye (nearsightedness). Risk Factors Genetics, nearsightedness. Prevention There are no known preventative measures. Treatments · Close monitoring every 1-2 years for development of a retinal hole or tear. · If a retinal hole or tear occurs; laser retinopexy surgery. Neither snail track nor lattice degeneration affect vision. Vision is only affected if the degeneration leads to a retinal hole or tear and then a retinal detachment. Holes and tears can usually be treated with retinal laser surgery without any affects on vision but if a retinal detachment occurs, long-term vision will be permanently affected. For either lattice or snail track degeneration, seek medical attention same day with any new flashes of light, floaters or a veil appearance in vision.

Dr Ben Wild For vision to be in clear and in focus, light must pass through the cornea, the clear tissue at the front of the eye, the pupil, the black hole in the center of the colored iris, and the lens, the clear tissue inside the eye, to the tissue responsible for detecting light, the retina. The lens sits inside a bag (capsule) attached to strings (zonules) that are controlled by muscles (ciliary body). Cataracts refer to the fogging/clouding of the lens and lead to decreased vision, poor night vision, and glare. A cataract, or the fogged lens, is treated with cataract surgery. In this surgery, a hole is created in the capsule at the front of the lens, the lens is then emulsified and vacuumed away, and an implant lens is inserted into the capsule. A healthy eye with an implanted lens after cataract surgery. Posterior capsular opacification (PCO), also known as 'after-cataract', occurs in about 20-25% of patients after cataract surgery. It can occur as little as 1 week after cataract surgery but often occurs a year or a few years after cataract surgery. It occurs when some of the biological cells from the natural lens (the cataract) are left in the capsule before the implant lens is placed. These cells attach to the implanted lens and start growing and multiplying. Interestingly, research shows that the design of the implanted lens has more impact on PCO development than the material of the lens. An eye with an implanted lens after cataract surgery with PCO. Signs Clear pearls of swollen natural lens cells or a fibrous layer of cells, on the back surface of the implant lens. Symptoms Slowly worsening vision, increasing glare, double vision coming from one eye, reducing contrast sensitivity. Causes Growth and multiplication of cells from the natural lens on the implanted lens. Risk Factors The design of the implanted lens, and to a lesser extent, the material of the implanted lens. Prevention There are no known preventative measures. Treatments Laser (Nd:YAG laser) capsulotomy where the surgeon dilates the pupils with eye drops, focusses a laser on the cells creating the PCO, and creates a hole in the back of the capsule so that there is no meshwork for the cells to adhere. Complications Complications of the laser capsulotomy are usually very rare but can include lens pitting (if the laser hits the implanted lens instead of the capsule) which rarely causes any issues, new floaters which dissipate over 4-6 weeks, mild/temporary increase in eye pressure, retinal tears or retinal detachments in highly myopic/nearsighted eyes, and swelling of the macula if attempted within 6 months of cataract surgery. PCO is easily treated with a simple 30 second to 1 minute laser treatment. If treated correctly, it should never return.

Dr Ben Wild Our vision comes from light waves stimulating retinal photoreceptors and these photoreceptors transferring their signals through the several different cells along the various layers of the retina and onwards to the brain. In order for light to focus on the retina, it must pass through the clear cornea at the front of the eye, the pupil, the clear lens and the clear vitreous humor gel before stimulating the retina. A frontal view of a healthy retina. A retinal detachment refers to an event where the retina separates from the retinal pigment epithelium, which separates the retina from the choroidal blood supply at the back of the eye, There are 3 main types or retinal detachments; 1. rhegmatogenous, where the detachment came from fluid entering a retinal hole or tear, 2. traction, where there are pulling forces on the retina but no retinal break, and 3. exudative, where there is a leak from the blood vessels of the retina, choroid or other tissue causing the detachment. Retinal detachments occur in 1 out of every 10,000 people, in 10% of those cases occur in both eyes at some point, and over 40% of retinal detachment patients are nearsighted where the higher the nearsightedness the higher the risk. A frontal view of a retina with a rhegmatogenous detachment (upper left), a tractional detachment (middle), and an exudative detachment (middle right). Signs Low eye pressure, inflammation inside the eye (uveitis), possible asymmetrical pupil reactions (RAPD), retinal break, retinal thinning, growth of fragile blood vessels, wavy moveable retina in rhegmatogenous, tent-like concave pulling on the retina in tractional, smooth convex shifting fluid in exudative, Symptoms Flashes of light like lightning bolts and floaters for rhegmatogenous, curtain-like blind spot for all 3 types, Causes Fluid entering the space between the retina and the retinal pigment epithelium. Risk Factors Prevention Avoid health conditions that can cause retinopathy by living a healthy balanced lifestyle, treat retinal breaks before they become retinal detachments. Treatments · Pneumatic retinopexy where the detachment is treated with laser or cryotherapy followed by the insertion of a gas or silicone bubble to hold the retina in place. · Scleral buckle (a silicone pad sutured to the sclera (white part of the eye), that compresses the eye), done after vitrectomy (removal of the vitreous gel). · Manually drain the fluid. A retinal detachment, once occurred, affects vision permanently. If the macula, the area of the retina that corresponds to a patient's central vision, is still attached, the surgery for retinal detachment needs to proceed asap (within 24 hours). If the macula has detached, there is less urgency because the damage has already been done. There is a considerable amount of variability in vision after a retinal detachment has been treated. Outcomes range from 20/25 vision with a permanent blind spot to legally blind. The sooner a retinal detachment is treated, the more likely the patient is to have some visual recovery.

Dr Ben Wild Our vision comes from light waves stimulating retinal photoreceptors and these photoreceptors transferring their signals through the several different cells along the various layers of the retina and onwards to the brain. A frontal view of a healthy retina. Retinoschisis is a condition where the layers of the retina start to separate from each other. It starts as tiny microcysts (pockets of fluid within the retina) that merge to create large areas of separation. Retinoschisis is seen in 5% of people, most of which are farsighted. There are 3 main types; degenerative, where the photoreceptor layer has separated, typical, where the outer plexiform layer (the layer next to the photoreceptors) has separated, and reticular, where the nerve fiber layer has separated. A frontal view of a retina with retinoschisis. Signs Smooth convex immobile dome of retina seen in both eyes 80% of the time, if there is a pigment line at the edge, there is likely also a retina detachment, white sclerosed blood vessels overtop, snowflake debris, microaneurysms, inner and/or outer retinal breaks. Symptoms Usually asymptomatic (no symptoms), very rare noticeable blind spot, rare vitreous hemorrhage/retinal detachment symptoms. Causes There are no known causes. Risk Factors Genetics, farsightedness. Prevention There are no known preventative measures. Treatments · Close monitoring every 1-2 years for size progression. · Laser retinopexy surgery with progression. · Vitrectomy surgery with vitreous hemorrhage (bleeding in the vitreous cavity). Retinoschisis is not usually a condition that affects vision or lead to any visual issues or even require surgery or treatment. It usually progresses slowly with very rare bleeding into the vitreous humor gel. In 1% of patients, a retinal detachment is possible and therefore careful monitoring is required.

Dr Ben Wild Our vision comes from light waves stimulating retinal photoreceptors and these photoreceptors transferring their signals through the several different cells along the various layers of the retina and onwards to the brain. In order for light to focus on the retina, it must pass through the clear cornea at the front of the eye, the pupil, the clear lens and the clear vitreous humor gel before stimulating the retina. A frontal view of a healthy retina. A retinal break is usually caused by pulling forced between the vitreous humor gel and the retina, also know as traction. 20% of all retinal breaks are observed after a symptomatic posterior vitreous detachment (flashes, floaters, etc.) which, briefly, is a normal occurrence due to age where the vitreous humor separates from the retina. These breaks can occur during the PVD or a few weeks afterwards. Retinal breaks can be sub-classified into horseshoe tears (where the retina is torn but is still attached to normal retina and vitreous gel), operculated holes/tears (where a clump of retina has been fully separated from the rest of the retina), and atrophic retinal holes (where there is a hole but no retina can be visualized in the vitreous). Less common retinal breaks include retinal dialysis and giant retinal tears. A frontal view of a retina with a horseshoe tear (upper left), operculated break with floater (middle left), and an atrophic hole with fluid (bottom left). Signs Bright red spot where the retina was torn, if fully torn then there may be an operculum, if the retina is still attached then there is a visible retinal flap. Symptoms Often asymptomatic (no symptoms), possible flashes of light like lightning bolts, possible large or very small floaters. Causes Usually vitreous humor pulling on the retina causing a tear. Risk Factors Genetics of thin retinas, nearsightedness, previous retinal break, Marfan Syndrome/Stickler Syndrome/Ehlers Danlos Syndrome, trauma, current posterior vitreous detachment, retinal tufts, lattice degeneration. Prevention There are no known preventative measures. Treatments · Monitor every 1-2 years if low risk of progressing to a retinal detachment. · Laser retinopexy surgery if high risk. · Cryoretinopexy surgery if high risk. A retinal break often does not affect vision except for the when it is formed (flashes, floaters, etc.). They often do not need treatment. When there is a risk of progressing to a retinal detachment, such as when there are flashes and floaters, when the break is large, when they are horseshoe in nature, and when they are located at the top of the eye (superior), surgery is warranted. Surgery can lower the chance of a retinal detachment from 90% after a symptomatic retinal break to 5% after surgery. There is a chance the surgery could cause a new retinal break so follow ups are necessary.

Dr Ben Wild The orbital fossa (eye socket) contains numerous tissues including the eye itself, optic nerve, muscles, fat, and much more. The contents of the eye sockets are protected from the elements and held inwards by a membrane called the orbital septum. This membrane extends from the skull to the eyelid margins. Frontal view of a healthy eye. Preseptal cellulitis refers to an infection anterior (in front of) the orbital septum deep in the skin of the eyelids. It is much more common than orbital cellulitis and is usually less worrisome, however, it may lead to more serious conditions such as orbital cellulitis, meningitis, or abscess formation. Frontal view of preseptal cellulitis showing red eyelids. Orbital cellulitis refers to an infection behind the orbital septum and can be both vision and life threatening. It is most commonly seen in children and usually stems from a sinus infection but can begin through a skin infection, after dental work, from preseptal cellulitis, dacryoadenitis and more. Frontal view of orbital cellulitis showing a violently red eye, red eyelids, and bulging eye. Signs Symptoms Causes Infection. Risk Factors Prevention Seek medical attention for skin, sinus, respiratory tract, and ear infections. Treatments Preseptal cellulitis is usually an easily treatable condition that requires about 10 days of antibiotics and is not contagious. Orbital cellulitis is vision and life threatening and does necessitate hospital admission and frequent follow ups but timely treatment can drastically increase the odds of a full recovery.

Dr Ben Wild The 3 main muscle groups in our body are skeletal muscles, which are attached to bones, cardiac muscles (heart muscles), and smooth muscles, which are found in body cavities, blood vessels, etc. All of these muscles are stimulated by the release of neurotransmitters from their associated nerves. There are many medical conditions that can affect muscle function. Myasthenia Gravis (MG) is an autoimmune condition where the body creates antibodies, similar to those that are created after getting the flu to help fight off the next exposure to the flu, but these antibodies attach to the receptors on skeletal muscle cells responsible for detecting the neurotransmitters that cause muscle contraction. With the antibodies stuck to these receptors, muscle cells can no longer detect neurotransmitters and therefore cannot be stimulated. MG can be classified as systemic (full body), bulbar or ocular. It can present as early as birth or as late as 7-8th decade of life. Symptoms may worsen with certain antibiotics or beta-blocker medications. MG affects the eye muscles first in 60% of all cases with the majority of affected patients complaining of episodes of drooping eyelids and/or double vision. On the left is a frontal view of a healthy eye and on the right, an eye showing a droopy eyelid, one of the signs of Myasthenia Gravis. Causes Autoimmune disease unknown origin. Risk Factors Female gender (2x more likely than men) Prevention There are no known preventative measures. Tests Droopy lids get worse after looking upwards for 60 seconds, eyelids shoot upwards after changing focus from looking down to straight ahead, droopy lids get better after 2 minutes of exposure to an ice pack, blood work, anti-cholinesterase response testing, electromyography, muscle biopsy. Treatments · Steroid pills. · Pyridostigmine. · Immunosuppressives. · Plasmapheresis to filter the blood of these antibodies. Symptoms are usually well managed with medication. Because MG is an autoimmune condition, it cannot, at this stage, be cured. After symptoms begin, it usually takes a few months for diagnosis and treatment to begin. It is recommended to see an optometrist as they may be able to put a temporary Fresnel prism on a pair of glasses to help with the double vision, which is likely to dissipate or be resolved after starting treatment.