Dr Ben Wild Our vision comes from light waves stimulating retinal photoreceptors and these photoreceptors transferring their signals through a multitude of other cells to the ganglion nerve cells. These ganglion cells bunch together and form the optic nerve. The optic nerve then sends the signal to the occipital lobe in the brain where vision is interpreted and recognized. An image of a healthy retina and optic nerve. Optic disk drusen are small calcified deposits that grow in the optic nerve. They occur in about 2% of people and 75% of the time are found in both eyes. Optic disc drusen are genetically inherited. Over time, these calcium deposits can grow and cut off the parts of the signal that goes from the optic nerve to the brain thus causing blind spots in 75% of cases. This condition has been known to correlate with higher chances of choroidal neovascularization (growth of small blood vessel networks), vein or artery occlusions, anterior ischemic optic neuropathy (inflammation of the optic nerve). An image of a healthy retina and optic disk drusen. Signs Blood vessels exiting the nerve are tortuous (wiggly), the nerve is lumpy and full, there may be more blood vessels exiting the nerve than normal, off-white lumps of calcium on the nerve that become easier to see during an eye exam with increased age. Symptoms Usually none, small blind spots may develop, on rare occasions, there may be episodes of blurry vision thought to be caused by decreased oxygen transfer to the optic nerve. Causes Genetically inherited in an autosomal dominant manner (only 1 copy of the trait is required). Risk Factors No known risk factors. Prevention There are no known preventative measures. Treatments There are no current treatments for optic nerve drusen but treatments are required for the conditions that are correlated with optic nerve drusen. · Intra-vitreal anti-VEGF injections for choroidal neovascularization (growth of small blood vessel networks). · Vitrectomy if there is a complicated blood vessel leak into the eye. · Glaucoma drops to decrease the chance of a second anterior ischemic optic neuropathy episode. Optic nerve drusen are quite common and in most cases do cause blind spots that slowly enlarge over time, much like those seen in glaucoma. Unfortunately, there currently are no treatments. Thankfully, unless complicated by one of the above secondary issues, this condition does not cause substantial vision loss and does not cause any discomfort.

Dr Ben Wild Our vision comes from light waves stimulating retinal photoreceptors and these photoreceptors transferring their signals through a multitude of other cells to the ganglion nerve cells. These ganglion cells bunch together and form the optic nerve. The optic nerve then sends the signal to the occipital lobe in the brain where vision is interpreted and recognized. An image of a healthy retina and optic nerve. Papilledema refers to the swelling of both optic nerves due to increased intra-cranial pressure (pressure in the skull leading to swelling of the brain). Intra-cranial pressure is regulated by the flow of cerebrospinal fluid between the brain and spinal cord. Any issue that affects how much fluid is created, how much is re-absorbed into the body, or the amount of free space there is in the skull can affect the pressure. Pressure changes usually cause headaches and sometimes, elevated intra-cranial pressure, can actually cause bilateral (both eyes) 6th nerve palsies leading to double vision. An image of a healthy retina and a swollen optic nerve. Signs Symptoms Headaches from elevated intra-cranial pressure can occur at any time of the day but are worse when elevating from a reclined position, on head tilt, coughing, and in rare cases, there are no headaches. Episodes of nausea, drowsiness, mild to no vision issues, double vision. Causes Increased intra-cranial pressure from idiopathic intracranial hypertension (IIH), elevated pressure of unknown cause often linked to weight gain, closed off brain ventricles (born like this, tumors, aneurysms, etc.), increased fluid from brain bleed, decreased absorption due to infection (meningitis), stroke, trauma, severely elevated blood pressure, side effects of birth control, certain antibiotics or other medications, and more. Risk Factors Poor health, overweight. Prevention There are no known preventative measures other than a healthy lifestyle. Treatments After confirming elevated intra-cranial pressure through brain imaging and lumbar puncture (measure the pressure of cerebrospinal fluid as it is extracted from the spinal cord): · Lose weight. · Discontinue medications that may be causing the condition. · Acetazolamide pills to decrease production of cerebrospinal fluid. · Diuretic (blood pressure) medication to remove excess fluid. · Brain surgery to remove masses or create shunts for better cerebrospinal fluid flow. Patients with papilledema usually do not suffer any long term visual defects unless it is not diagnosed or treated properly at first onset. If the optic nerve swelling takes too long to resolve, permanent blind spots start to form and visual acuity may be affected.

Dr Ben Wild Our vision comes from light waves stimulating retinal photoreceptors and these photoreceptors transferring their signals through a multitude of other cells to the ganglion nerve cells. These ganglion cells bunch together and form the optic nerve. The optic nerve then sends the signal to the occipital lobe in the brain where vision is interpreted and recognized. An image of a healthy retina and optic nerve. This is also noticed in retrobulbar optic neuritis because the inflammation is contained behind the eye. Optic neuritis refers to inflammation of the optic nerve thereby affecting the transfer of vision from the eye to the brain. It is extremely rare to see this bilaterally (in both eyes). The different presentations of optic neuritis include retrobulbar (inflammation of the optic nerve behind the eye), papillitis (inflammation of the optic nerve inside the eye), and neuroretinitis (inflammation of the brain extending into the optic nerve and the retina inside the eye). The top image shows optic nerve swelling and retinal hemorrhages consistent with a papillitis, the bottom image shows the same inflammation plus swelling of the macula (darker area) in neuroretinitis. Signs Symptoms Causes Risk Factors Prevention There are no known preventative measures other than reduce exposure to cats and ticks. Treatments

Dr Ben Wild Our eyes are complicated systems. 7 out of the 12 cranial nerves that help control the entire body affect the eyes or muscles around the eyes in some shape or form. There are several large areas in the brain dedicated to vision interpretation, eye muscle movements, and recognition. Any disruption to these pathways can cause difficulty with vision, eye muscle teaming, or even difficulty understanding what you are seeing. Multiple Sclerosis (MS) is a long lasting autoimmune condition characterized by the body’s defense system, the immune system, attacking the myelin sheath of it’s own neurons. The myelin sheath is a coating seen on some neurons, the white matter of the brain and several other nerves, that helps insulate the neuron and speed up signal transduction. This is a progressively worsening condition that has hugely variable prognoses. In terms of how MS affects the eyes, 30% of MS diagnoses come after first presenting as optic neuritis (inflammation of the optic nerve). This results in pain around the eye that’s worse on eye movement, asymmetrical pupil reactions to light, decreased vision in one eye, abnormal color vision, and enlarged blind spots in one’s vision. 50% of patients with MS have had at least 1 episode of optic neuritis. If MS affects the brainstem, the affected patient could notice double vision or nystagmus (oscillating eyes) and if it affects cerebrum of the brain it can cause a hemianopia (loss of half of the field of view to a blind spot). Double vision comes from either a loss of function of the 3rd cranial nerve (the affected eye would appear to be looking down and away, have a droopy eyelid and maybe a dilated pupil) or internuclear ophthalmoplegia (the affected eye cannot abduct (move away from the nose), and when looking the opposite way, has a nystagmus). An image of a healthy retina and optic nerve. This is also noticed in retrobulbar optic neuritis (the most common optic neuritis associated with MS) because the inflammation is contained behind the eye. Signs Episodes of impaired muscle function, abnormal pupil reflexes to light, impaired language and emotional functions, impaired coordination and balance. Symptoms Blurred or doubled vision, abnormal color vision, pain and loss of vision, trouble walking, numbness, pain or tingling of fingers/toes, muscle weakness in arms and legs, muscle spasms, speech problems, tremors, hearing loss, dizziness. Causes Autoimmune inflammation of the myelin sheath on nerves. Risk Factors Infectious agents of unknown origin, unknown environmental factors, genetics. Prevention There are no known preventative measures. Treatments After confirming diagnosis with an MRI, cerebrospinal fluid analysis and blood tests; · Immunotherapy to decrease rate of progression. · Canes, braces, walkers for mobility. · Rehabilitation activities. There are no known cures for MS at this time. The prognoses for MS are hugely variable. Some individuals only ever show mild symptoms, other individuals lose the ability to walk, become paralyzed, incontinent, have breathing difficulty, lose the ability to swallow, and more. Thankfully, researchers are currently working on strategies to greatly lower the rate of progression of MS in affected patients.

Dr Ben Wild Our vision comes from light waves stimulating retinal photoreceptors and these photoreceptors transferring their signals through a multitude of other cells to the ganglion nerve cells. These ganglion cells bunch together and form the optic nerve. The optic nerve then sends the signal to the occipital lobe in the brain where vision is interpreted and recognized. An image of a healthy retina and optic nerve. Non-arteritic ischemic optic neuropathy (NAION) occurs when the blood vessels behind the eye, responsible for maintaining the optic nerve’s health, occlude. This cuts off blood supply to the nerve and damages the nerve. It occurs unilaterally (in one eye) but can occur in the other eye at a later date. It usually occurs over the age of 50 but does not usually occur in advanced ages. An image showing optic nerve swelling and retinal hemorrhages consistent with a NAION. Signs Optic nerve redness and swelling, broken blood vessels around the nerve, if longstanding, the nerve starts to atrophy (die off) and becomes pale white. Symptoms Sudden painless vision loss usually after waking up, blind spot on the bottom or top half of vision, decreased vision. Causes Occluded posterior ciliary artery (one of the several that nourishes the optic nerve behind the eye). Risk Factors High blood pressure, diabetes, high cholesterol, cardiovascular disease, anti-phospholipids antibody syndrome, hyperhomocysteinemia, sleep apnea, cataract surgery, birth control, medications for erectile dysfunction. Prevention There are no known preventative measures other than a healthy lifestyle. Treatments · There are currently no known treatments. The optic nerve swelling in NAION will decrease over time but will result in atrophy of the nerve. Visual acuity and blind spots will typically improve over time with 50% of patients reaching vision 20/30 or better but 25% of patients never exceed 20/200 or legally blind. There is a 15% chance of it occurring in the other eye within the proceeding 5 years.

Dr Ben Wild Our vision comes from light waves stimulating retinal photoreceptors and these photoreceptors transferring their signals through a multitude of other cells to the ganglion nerve cells. These ganglion cells bunch together and form the optic nerve. The optic nerve then sends the signal to the occipital lobe in the brain where vision is interpreted and recognized. An image of a healthy retina and optic nerve. Arteritic ischemic optic neuropathy (AION) occurs due to an autoimmune condition called Giant Cell Arteritis (GCA) that causes inflammation in large and medium arteries within the body. This inflammation can lead to the decay of arteries such as the aorta around the heart, the temporal artery above the eye and ear, the ophthalmic artery inside the optic nerve, along with many others. AION usually occurs in the elderly with an average age around 70 years old and has an unknown connection to polymyalgia rheumatica, a secondary diagnosis 50% of the time. An image showing a swollen optic nerve consistent with AION. Signs White swollen nerve. Symptoms Causes Autoimmune inflammation of medium and large arteries caused by GCA. Risk Factors Female gender, increased age, Caucasian decent, polymyalgia rheumatica, genetics. Prevention There are no known preventative measures. Treatments · Intravenous steroids. · Antiplatelet therapy. · Immunosuppression therapy with methotrexate. Vision loss is usually permanent but prompt treatment may lead to partial recovery and may protect the fellow eye from losing vision.

Dr Ben Wild For light to stimulate the retina (the part of the eye that detects light), it must pass through a clear cornea (front of the eye), the pupil (the hole in the colored part of the eye also known as the iris), the clear lens inside the eye and through clear gel called the vitreous humor. The vitreous humor is a gel composed of collagen, proteins, hyaluronic acid and water and acts as scaffolding for the eye, helps transfer nutrients to the different structures within the eye and helps keep the eye inflated. Sagittal view of a healthy eye. Asteroid hyalosis is a degenerative process that occurs when calcium pyrophosphate salt particles accumulate in the vitreous humor. About 3% of people over the age of 75 have some sign of asteroid hyalosis. In the vast majority (75% of cases) this occurs unilaterally (in one eye). It is still uncertain what the origin of these salt crystals are or why it occurs. Sagittal view of an eye with crystals, signifying asteroid hyalosis, floating in the vitreous gel. Signs Off white to yellow crystals suspended in or floating within the vitreous humor. Symptoms Usually no symptoms, sometimes patients see many small floaters in their vision. Causes Still unknown. Risk Factors Male gender. Prevention There are no known preventative measures. Treatments · Vitrectomy (surgical removal of vitreous humor). Asteroid hyalosis is not known to be associated with any other health conditions or cause damage to the eyes. It is very rare that enough crystals accumulate to affect vision but if that does occur, vitrectomy surgery can clean out the vitreous humor.

Dr Ben Wild Eye movements are controlled by 6 extra-ocular muscles. The superior rectus (SR) pulls the eye upwards, the inferior rectus (IR) pulls the eye downwards, the lateral rectus (LR) pulls the eye outwards and the medial rectus (MR) pulls the eye inwards. The superior oblique (SO) muscle connects to the eye after passing through a pulley called the trochlea and is mainly responsible for rotating the eye inwards and pushing the eye downwards. The inferior oblique (IO) follows a similar path as the superior oblique, except underneath the eye and does not travel through a pulley system. Duane retraction syndrome refers to a congenital condition (born like this) where the 3rd cranial nerve, the nerve that controls the SR, IR, MR and IO muscles also controls the LR which is supposed to be under sole control of the 6th cranial nerve. When these two nerve signals fight each other, the eye retracts into the orbit. Frontal view of a right eye with extra-ocular eye muscles. The highlighted muscles indicate the medial and lateral rectus muscles that battle each other in Duane Retraction Syndrome. There are 3 main types of Duane retraction syndrome. All 3 types are sometimes unilateral (one eye) but often bilateral (both eyes). Often there are other systemic deficits like external ear abnormalities, speech disorders, skeletal abnormalities. Type 1 is the most common and occurs when there is no 6th nerve control of the LR muscle but the 3rd nerve has partially grown in its place. This patient cannot abduct the eye (look away) and when trying to do so, the eye retracts. This patient may have a crossed eye. Type 2 is the least common and occurs when the 6th nerve is intact and present but the 3rd nerve still has some control over the LR muscle. In this case the patient can’t adduct the eye (look inwards). This patient may have a wondering eye. Type 3 has almost no 6th nerve control and the 3rd nerve equally controls the LR and MR muscle. This patient cannot look left or right and when trying to do so, the eye retracts. Signs Head turn to reduce possible double vision, difficulty moving the eye out (type 1 and 3), difficulty moving the eye in (type 2 and 3), retraction of eye into orbit. Symptoms Usually no symptoms, sometimes patients may notice double vision and pain/tenderness in up and inwards gaze. Causes Congenital malformation. Risk Factors There are no known risk factors. Prevention There are no known preventative measures. Treatments · No treatment required in most cases. · Surgery to straighten head posture or for double vision. Duane retraction syndrome may restrict a patient’s life in terms of certain career choices (pilot, truck driver, etc.) but is not vision threatening. In most cases the patient suppresses (brain ignores) one eye when the eyes are not aligned to avoid double vision and therefore the patient is unaware of any issue. In some cases surgery is needed to correct any double vision or fix a tilted head posture but surgery does not correct the congenital malformation, just the double vision or head posture.

Dr Ben Wild Eye movements are controlled by 6 extra-ocular muscles. The superior rectus pulls the eye upwards, the inferior rectus pulls the eye downwards, the lateral rectus pulls the eye outwards and the medial rectus pulls the eye inwards. The superior oblique muscle connects to the eye after passing through a pulley called the trochlea and is mainly responsible for rotating the eye inwards and pushing the eye downwards. The inferior oblique follows a similar path as the superior oblique, except underneath the eye and does not travel through a pulley system. A frontal image of a right eye with the extra-ocular muscles. If any of these muscles are too tight, too loose, too strong or too weak, there is the potential for an eye turn (strabismus). Strabismus can occur when one of these muscles is either working too hard or not hard enough and an eye turn is noticed. Exotropia is a wandering eye, esotropia is a crossed eye, hypotropia is one eye is looking downwards and hypertropia is one eye is looking upwards. Normally, the eye muscles are able to focus the eyes very closely to a single target. When the images from each eye are similar, a fusion reflex kicks in so that the person can see a single target with depth (3 dimensions instead of 2). When the muscles are unable to align both eyes towards a single target, the fusion reflex is unable to activate, and the patient either has double vision or the patient’s brain suppresses (ignores) the image from one eye to avoid double vision. Other ways to avoid double vision is adopting a head tilt or turn, raising the chin or lowering the chin. Pseudo-strabismus occurs when one eye looks like it is not pointing in the same direction as the other but it actually is. This is common in babies. Babies have an extra fold of skin called the epicanthal fold that can sometimes make an eye look crossed. Also, if the distance between the eyes is either very narrow or very wide, the eyes can look crossed or wandering. A normal pair of eyes looking off into the distance. An image showing the right eye is turned inwards. This is an esotropia style of strabismus. Signs One eye looking in a different direction compared to the other eye. Head tilt, head turn, raised chin or lowered chin. Symptoms Possible double vision, lack of depth perception. Causes One or more muscles not working hard enough or working too hard. Risk Factors Difference in prescriptions between the two eyes (anisometropia), different image sizes between the two eyes (aniseikonia), decreased vision due to eye problem (cataract, corneal scar, retinal degeneration, etc.), congenital malformation. Prevention 1st eye exam around 1 year old followed by another at 3-4 years old to ensure proper development of the eyes and eye muscles. Early intervention if issues arise. Treatments · Treat any cause for decreased vision. · Glasses or contacts after a cycloplegic refraction (prescription done after dilating drops). · Treat lazy eye by patching good eye 2hrs/day to full time. · Vision therapy (eye exercises to regain proper eye muscle control). · Surgery by age of 1 or 2 if born with strabismus or upon 1st discovering a strabismus is constant (doesn’t come and go). If born with strabismus, surgery can align the eyes but the patient may need several re-alignment surgeries in their lifetime. There is also only a slim chance of gaining depth perception. If the strabismus develops after the age of 3-4, full glasses prescription and vision therapy can often correct the alignment issue, and if not, surgery can re-align the eyes. Regaining depth perception in this case is likely but not promised. For pseudo-strabismus, as babies grow and lose their epicanthal eyelid folds, their eyes will look aligned.

Dr Ben Wild Our vision comes from light waves stimulating retinal photoreceptors and these photoreceptors transferring their signals through a multitude of other cells to the ganglion nerve cells. These ganglion cells bunch together and form the optic nerve. The optic nerve then sends the signal to the occipital lobe in the brain where vision is interpreted and recognized. Amblyopia refers to a condition where the vision is sub-optimal despite a healthy eye. It is now known to be caused by the improper development of the visual system within the brain. The other term for this is a “lazy eye”. Amblyopia is usually unilateral (affects one eye) but sometimes bilateral (both eyes). Signs There are no signs of amblyopia other than slower brain transmission of visual information only noticed in highly specialized visual evoked potential testing. Symptoms Decreased vision. More difficulty recognizing letters in a row than the same letters one by one. Causes Visual deprivation (congenital cataract, corneal scar, retinal dystrophy, droopy eyelid, etc., blocking vision so the brain never develops the vision in that eye), strabismic (one eye is turned and to avoid double vision the brain does not develop the vision in that eye), anisometropic (one eye has a prescription so different from the other that the brain only develops the vision from one eye), ametropic (the prescription is so high in both eyes that the visual system did not develop properly). Risk Factors High prescription is one or both eyes, congenital cataracts, droopy eyelid, corneal scars, retinal dystrophy, congenital malformations, strabismus (eye turn). Prevention 1st eye exam around 1 year old followed by another at 3-4 years old to ensure proper development of the eyes and visual system. Treatments · Occlusion of the good eye to force the patient to use their poor eye and force the brain to develop the visual pathways (only effective until teenage years). · Penalization of the good eye by making it blurry with the use of filters on glasses or atropine eyedrops. · Vision therapy involving games that can only be played if the player is using both eyes. Amblyopia is manageable at early ages. In most instances, glasses alone can improve vision in the weaker eye, or in both eyes, significantly within a few months. In some cases, occlusion or penalization of the good eye is required between 2 hours a day and all day. Vision therapy with games requiring the use of both eyes has shown immense promise in being the best solution and seems to be able to improve vision in the worse eye even in adulthood.

Dr Ben Wild Our eye muscles are all interconnected in a complicated pathway with a common goal of delivering comfortable vision in any gaze and at any distance. To have comfortable near vision, the medial rectus muscles of each eye must pull the eyes inwards (converge the eyes), the pupils must shrink to help with depth of field, and the ciliary body, a muscle inside the eye, must constrict to change the shape of the lens inside the eye to focus the light from the near target on the retina. Frontal view of a right eye with the extra-ocular muscles attached. The highlighted muscle represents the medial rectus muscle required to pull the eyes inwards (converge). Convergence insufficiency is a condition whereby the medial rectus muscles of each eye are working well when looking at distant objects but have a hard time pulling the eyes inwards for near targets. Signs Inability to converge (or cross) the eyes. Symptoms Eye strain after near work, double vision at near, loss of depth perception when looking at a near target, skipping words when reading, re-reading the same line in a book, headaches after near work, blurred vision, jumping words on a screen or a page. Causes The causes are unknown but there are many risk factors and correlated factors with convergence insufficiency. Risk Factors Concussion, traumatic brain injury, convergence fatigue (can converge well but, after a while, the muscles tire out), Grave’s disease (thyroid related), Myasthenia Gravis, Parkinson’s, Alzheimer’s, accommodative insufficiency. Prevention Allow children to crawl and develop their near vision, avoid head trauma, apply the 20-20-20 rule (after 20 minutes of near work look at a target at least 20 feet away for 20 seconds). Treatments · Vision therapy including eye exercises that stimulate gradual convergence (pencil push ups, Brock string, etc.), jump convergence (Brock string, Hart Chart, etc.), prism training to simulate change in focal distance, computer-based training, in office-based training, and many more. · Seek out an optometrist who specializes in vision therapy. · Surgery as last resort. When not associated with a systemic health condition or traumatic brain injury, convergence insufficiency exercises have an 80% success rate at eliminating all signs and symptoms. When associated with a traumatic brain injury, exercises may still help but take much longer and require more dedication. When associated with systemic diseases, exercises will actually tire out the muscles and make the symptoms worse without providing any future benefit.

Dr Ben Wild Eye movements are controlled by 6 extra-ocular muscles. The superior rectus pulls the eye upwards, the inferior rectus pulls the eye downwards, the lateral rectus pulls the eye outwards and the medial rectus pulls the eye inwards. The superior oblique muscle connects to the eye after passing through a pulley called the trochlea and is mainly responsible for rotating the eye inwards and pushing the eye downwards. The inferior oblique follows a similar path as the superior oblique, except underneath the eye and does not travel through a pulley system. A frontal image of a right eye with the extra-ocular muscles. If any of these muscles are too tight, too loose, too strong or too weak, there is the potential for an eye turn (strabismus). Esotropia is a type of strabismus (eye turn) where one eye is seen crossing inwards compared to the other but all of the eye muscles still have full range of motion. There are many different causes of esotropia and each has a different treatment and prognosis. Infantile esotropia is made apparent within the first 6 months after birth in an otherwise healthy child. Accommodative esotropia usually presents around 3-4 years old and is due to either uncorrected farsightedness or the accommodative system working too hard to see up close. Consecutive esotropia may occur after a surgery to correct the eye turn. Other types include basic esotropia that can develop at any age, convergence excess esotropia where the eye turn is only noticed when looking at something close, and divergent insufficiency esotropia where the eye turn is only noticed when looking far away. A normal pair of eyes looking off into the distance. An image showing the right eye is turned inwards. This is an esotropia style of strabismus. Signs One eye is turned inwards compared to the other. It may be constant or intermittent (comes and goes), it may be dependent on where the patient is looking, it may just be one eye or it may alternate eyes. Symptoms Possible double vision, lack of depth perception. Causes Birth anomalies, uncorrected farsightedness, developmental delays. Risk Factors Family history of strabismus. Prevention 1st eye exam around 1 year old followed by another at 3-4 years old to ensure proper development of the eyes and eye muscles. Treatments · Glasses or contacts after a cycloplegic refraction (prescription done after dilating drops). · Treat any amblyopia (lazy eye) by patching the good eye 2hrs/day to full time. · Vision therapy (eye exercises to regain proper eye muscle control). · Surgery by age of 1 or 2 if born with strabismus or upon 1st discovering a strabismus is constant (doesn’t come and go). If born with strabismus, surgery can align the eyes but the patient may need several re-alignment surgeries in their lifetime. There is also only a slim chance of gaining depth perception. If the strabismus develops after the age of 3-4, full glasses prescription and vision therapy can often correct the alignment issue, and if not, surgery can re-align the eyes. Regaining depth perception in this case is likely but not promised.