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- Migraines and the Eye
Dr Ben Wild Historically, it was thought that migraines, which are episodes of moderate to severe head pain, were due to fluctuations in blood flow to the brain. These were thought to occur due to blood vessel spasms. Current literature is now thinking that the spasms occur after the onset of the migraine. There are many different types of migraines but 4 types that affect the eyes directly include ocular migraine, migraine with aura (classical migraine), retinal migraine and ophthalmoplegic migraine. Other migraines affect the eyes indirectly as light sensitivity, pressure sensations, etc. Ocular migraines are very common and occur at least once in most people at some point in their lifetime. An ocular migraine is an aura that affects both eyes but sometimes seems like it only affects one. Example; it affects the right side of your vision in both eyes thereby appearing to only affect your right eye. These auras can appear as heat haze, pixelated vision, blind spots, tunnel vision, or scintillations that last between 5-30 minutes or many short episodes one after another. In this case, there is no headache or any other symptoms. A picture of a mountain range in Banff showing 3 different types of auras. 1) the rainbow of colors, may look like a kaleidoscope or may look pixelated, or may look like shimmers, 2) blur spot that may actually represent a full temporary blind spot, 3) translucent white apparitions that can take on any shape or form. Classical migraines often start with a visual aura that lasts 5-30. Unilateral auras are uncommon. About an hour after the aura a headache starts and nausea and light sensitivity may ensue. For diagnostic purposes, these symptoms must be reversible, the auras last over 4 minutes or a patient has many short auras, auras do not last over an hour, and a headache starts 1 hour after the aura. Retinal migraines affect 1 eye only and are thought to be due to blood vessel spasms around the eye. This occurs usually in young women but is rare. It is often associated with Raynaud’s (a circulatory disease), retinal emboli (strokes in the eye) and recurrent episodes may actually lead to permanent vision loss. Ophthalmoplegic migraines usually start around the age of 10 and are recurrent in nature. During an episode, the patient develops a 3rd nerve palsy and loses control of most of their eye muscles. This has been associated with demyelinating diseases like Multiple Sclerosis. Causes It used to be believed that migraines were blood vessel spasms but new research shows it is more complicated. Unknown. Risk Factors Sudden change in light (light to dim or vice versa), strong smells, loud noises, stress, caffeine, alcohol, chocolate, cheese, birth control, lack of sleep, fasting. Prevention Eliminate exposure to risk factors. This is easiest done by journaling every episode and writing down what was eaten or what occurred before the migraine. You may consider low dose analgesics to reduce recurrence. Treatments · Analgesics like Tylenol/aspirin. · Prescription strength analgesics. Migraines are a common and debilitating illness. There is no known physiological cause but there are many different risk factors and possible triggers. Apart from reducing exposure to these triggers, taking analgesics during an episode or to help decrease the recurrence rate of episodes, a patient usually suffers with migraines for the majority of their life. In some cases, migraines do disappear and in other cases they may go into remission only to return several years later. It’s important to talk to your family doctor about any moderate to severe headache.
- Scleritis
Dr Ben Wild The sclera is the white layer of the eye. Its function is as a strong barrier that holds the contents of the eye. It extends from the cornea to the optic nerve at the back. Frontal view of a healthy eye. Scleritis refers to inflammation and swelling of the sclera. It is commonly categorized into anterior non-necrotizing, anterior necrotizing, and posterior scleritis. Symptoms range from mild to severe. Anterior non-necrotizing is the most common and appears either as spread out (diffuse) or as nodular (large bump). Diffuse commonly associates with autoimmune conditions and progresses with symptoms worsening over days. It tends to reoccur on average every 6 years. Nodular is more commonly caused by infectious agents. It progresses slower and can last up to 6 years. Anterior necrotizing scleritis is the most aggressive. It typically affects older individuals, is caused by severe infections or end stage autoimmune diseases, results in extreme pain, and profound vision loss. Posterior scleritis can be seen alongside anterior scleritis or on its own. It is usually found with other retrobulbar inflammatory conditions (conditions that affect the back of the eye) such as optic neuritis, inflammation of the eye muscles (myositis), and more. Ultrasound may be needed for diagnosis. Frontal view of an eye with necrotizing scleritis on the left of the picture and diffuse scleritis on the right. Signs Symptoms Causes Inflammation of the sclera. Risk Factors Infectious (herpes zoster virus, tuberculosis, Leprosy, syphilis, Lyme, fungus and more), autoimmune disease (rheumatoid arthritis, Wegner’s granulomatosis, polyarteritis nodosa, polychondritis, sarcoidosis, ankylosing spondylitis, etc.). Prevention Treat infections timely and use prophylactic immune modulating medications when there is an auto-immune condition. Treatments · Determine cause via blood work, chest x-ray, sinus/joint imaging, orbital CT scans, ultrasound imaging or biopsy for infection. · Artificial tears for very mild. · Steroid eye drops for mild. · Non-steroidal anti-inflammatory pills for mild. · Steroid injection for moderate. · Steroid pills for severe. · Disease modifying anti-rheumatic drugs for severe. Anterior non-necrotizing scleritis is usually recurrent and leads to thinning of the sclera, turning the sclera blue, and permanently dilated blood vessels but does not cause any further morbidity or affect vision. Necrotizing scleritis can be vision threatening and is even associated with a 5-year mortality rate of 50-60% if caused by an auto-immune disorder. If not treated promptly, it can lead to the loss of the eye or death. Posterior scleritis can lead to retinal detachments, choroidal detachments, optic neuritis or swelling and other conditions that cause permanent vision loss even if treated promptly.
- Thygeson's SPK
Dr Ben Wild The cornea is the outermost layer of the eye in front of the iris. It is a clear tissue, void of any blood vessels, and is one of the main optical components responsible for focusing light on the retina. Frontal view of a healthy eye. Thygeson’s superficial punctate keratitis (SPK) is a condition that affects the cornea of each eye. It usually presents in early adulthood but can affect anyone. It is a fairly uncommon condition that does not have a known cause but is believed to be caused by a viral infection or auto-immune reaction. It occurs bilaterally and presents as a recurrent infection that then proceeds into a period of remission. Frontal view of an eye with Thygeson's SPK (grey dots on cornea). Signs Grainy appearance to the cornea with white/grey elevated dots in an eye that is not red. Symptoms Recurrent irritation, light sensitivity, blurred vision, tearing. Causes It is thought to be caused by an unknown virus but this has not been verified. Risk Factors Viral infection. Prevention There are no known preventative measures. Treatments · Artificial tears for comfort. · Bandage contact lens. · Steroid drops for active infection. · Cyclosporin drops to lower lengthen remission time. · Phototherapeutic keratectomy to get rid of scarring. Thygeson’s SPK is a condition that can last for 1-2 months followed by a 6-week remission period before returning. In most cases, this condition follows this pattern for 4 years before disappearing for good but some cases have been reported to last over 40 years. It can affect vision but usually is not vision threatening.
- Refractive Eye Surgeries
Dr Ben Wild The retina, located on the innermost portion of the back of the eye, senses light that later gets processed into vision by the brain. For clear vision, the light must be well focused on the retina. The cornea, the clear, outermost structure at the front of the eye and the lens, another clear structure located behind the iris, visible through the pupil, are the two structures that focus the light on the retina. A person is nearsighted if the cornea or lens is too strong or the eye is too long and a person is farsighted when the cornea or lens is too weak or the eye is too small. Refractive eye surgery refers to a collection of surgeries that change the power of either the cornea or the lens. Laser eye surgery either strengthens or weakens the power of the cornea by changing its shape with the use of a laser. Refractive lens exchange (RLE) replaces the natural lens inside the eye with a plastic lens of appropriate strength. Implantable collamer lens (ICL) surgery changes the focusing power of the eye by adding a plastic lens behind the iris but in front of the natural lens. To the left is a picture showing a healthy cornea, represented in blue on the left and lens represented as a semi transparent oblong lenticule on the inside of the eye on the right. Lasik is the most common laser eye procedure. It starts with a suction ring being applied to the eye to flatten the eye. A laser or a blade is then used to create a thin flap on the front of the cornea as demonstrated in the picture to the left. The flap is then lifted up and a laser is used to reshape the cornea. The flap is then lowered and recentered. Lasik can correct up to 4 Diopters (D) of hyperopia (farsightedness), 5D of astigmatism and 12D of myopia (nearsightedness) depending on the thickness of the cornea. It offers greater post-operative comfort, fast recovery time, and minimal haze formation. Intraoperative complications include errors in creating the flap and post-operative complications include dry eyes, wrinkling or dislocation of the flap, haze causing glare, growth of the corneal epithelium underneath the flap, inflammation, bacterial keratitis, and corneal ectasia (see corneal ectasia for more information). Photorefractive keratectomy (PRK) is an older laser eye surgery technique whereby, instead of creating a flap, the surgeon removes the corneal epithelium (top layer of the cornea) with alcohol, scrubber or sponge and uses a laser to reshape the cornea. A bandage contact lens is then inserted onto the eye so that the epithelium can regrow (2-3 days). PRK can correct minor amounts of hyperopia, 3D of astigmatism, and 6D of myopia. It is a safer option for patients with thin corneas and there is less risk of serious intra and post operative complications. It is best for patients with risky jobs, corneal dystrophies (see corneal dystrophies for more information), prior laser surgery, and large pupils. It does however have a much slower recovery period and unpredictable post-operative discomfort, greater chance for haze formation and glare, decreased night vision and haloes for months, regression of prescription, abnormal healing, irregular astigmatism that cannot be fixed with glasses, inflammation and infections. Small incision lenticule extraction (SMILE) surgery is the 3rd most common laser procedure quickly gaining popularity. It involves using a laser to form a removable piece of cornea in the shape of a lens and removing this piece through a small incision. It removes the risk of flap complications with Lasik but maintains all of the benefits of Lasik. There is evidence it causes less neurological damage thus reducing dry eye symptoms, and lowers infection rates. RLE changes the power of the eye by changing the strength of the lens. It is basically cataract surgery before cataracts develop. The surgeon creates 2 incisions in the cornea for his instruments, opens the natural capsule that contains the lens, separates the lens into many small pieces, vacuums up the lens fragments, inserts the plastic lens into the natural lens capsule, and closes the incisions. The plastic lens can correct a patient for either distance or near (single vision lens) or both (multifocal lens). Please note: multifocal lenses can enable patients to forgo the need for glasses altogether but cannot provide vision quite as sharp as single vision lenses and may cause permanent glare and haloes. RLE has all of the same complications as cataract surgery. This procedure is ideal for patients who have already gone through presbyopia (50 years of age or older). ICL surgery alters the strength of the eye by inserting an additional lens into the eye. It starts with the surgeon creating an incision in the cornea. A plastic lens is then inserted past the entrance of the pupil in front of the natural lens. In some instances, a laser is used to create a hole in the iris before surgery to ensure eye pressures do not elevate post-operatively. ICL is best suited for hyperopes or myopes with thin corneas. Complications are similar to those of cataract surgery plus the added risk of the plastic lens rubbing against the natural lens causing a cataract or elevated eye pressures progressing to glaucoma.
- Juvenile Idiopathic Arthritis and the Eye
Dr Ben Wild Juvenile idiopathic arthritis (JIA) is the most common systemic disease associated with anterior uveitis in childhood. Normally, the anterior chamber of the eye, which extends from the inner layer of the cornea to behind the iris, is void of any signs of inflammation. In anterior uveitis, fibrous debris and white blood cells are seen either stuck to the inner cornea or floating around in the anterior chamber of the eye. Frontal view (left) and sagittal view (right) of a healthy eye. JIA occurs in 1 in every 1000 people and represents an arthritis of unknown cause. It typically becomes symptomatic before the age of 16. Oligoarticular JIA includes inflammation of 4 joints or less, typically involves the knees, ankles and wrists, and usually presents at the age of 2. Polyarticular JIA involves over 5 joints and can present with rashes. Both types can present with uveitis but oligoarticular is more common. Still’s disease includes fever, rash, swollen lymph nodes, swollen liver and spleen and inflamed joints. Frontal view (left) showing synechiae (areas where iris is stuck to the lens) and sagittal view (right) showing white blood cells, fibers and the iris stuck to the lens. Signs There are not usually any signs that can be seen without specialized equipment. With this equipment, signs include white blood cells floating in the eye, white blood cells stuck to the inside of the cornea or to the iris, fibers floating around the anterior chamber, elevated eye pressures, iris stuck to the lens of the eye. With increased age; clouding of the cornea, cataracts, swelling of the retina, glaucoma. Symptoms Usually, no symptoms but there is a small chance of episodes of mild light sensitivity and/or pain. Causes Genetic immune system response against various joint and eye structures. Risk Factors The presence of auto-immune markers in the blood like anti-nuclear antigen, HLA-B27 proteins, and rheumatoid factor. Prevention There are no known preventative measures. Treatments · Follow up eye exams every 3, 6 or 12 months depending on age and which auto-immune markers are found in the blood. · Steroid drops or ointments. · Cyclogyl dilating drops. · Steroid injections. · Steroid pills. · Non-steroidal anti-inflammatory pills. · Disease modifying anti-rheumatic drugs. Progression of uveitis associated with JIA towards a state of blindness has historically been very likely but has been quickly down trending with better access to eyecare in developed countries. Early detection of uveitis is necessary but difficult as most cases do not present with any symptoms. Frequent follow ups are therefore required and can drastically reduce the chances of blindness.
- Infectious Keratitis
Dr Ben Wild The cornea is the outermost layer of the eye in front of the iris (the colored part of the eye). It is a clear tissue, void of any blood vessels, and is one of the main optical components responsible focusing light on the retina. Infectious keratitis occurs when a microbe (bacteria, fungus, or protozoa), or virus infects at least one of the layers of the cornea. A frontal view of a healthy eye. Bacterial keratitis is due to either Gram (+) or Gram (-) bacteria. Swabbing and culturing the bacteria can help in identification and treatment. Fungal keratitis is broken down into yeasts or filamentary fungal infections. They take longer to infect the cornea but tend to be much more symptomatic. Protozoa keratitis is caused by the Acanthamoeba organism. It is the most difficult to treat of all keratitis’ and often most symptomatic but is also the most rare. Viral keratitis’ vary greatly depending on which virus infects the eye. From the cold sore virus to the common cold virus and many more in between. They can infect all layers of the cornea and most typically don’t respond to treatment but do resolve on their own. Bacterial corneal ulcer (top left), filamentary and yeast ulcers (top right), ring ulcer from protozoa (bottom left), dendrite and punctate keratitis from 2 different viruses (bottom right). Signs Symptoms Causes Infection by bacteria, fungus, protozoa or virus. Risk Factors Contact lens wear (much higher risk if sleeping in lenses), contaminated water or soil in the eyes, skin conditions such as atopic dermatitis, rosacea, etc., malnutrition, immunodeficiency, blepharitis, trauma, diabetes, vitamin A deficiency. Prevention Proper contact lens wear and disposal. Proper eye and eyelid hygiene. Treatments Common: discontinue contact lens wear, throw out contact lenses, case, solution and makeup that touches the lids. Change to daily contact lenses. Steroid eye drops if infection is associated with ulceration, uveitis or scleritis. Avoid steroids in cold sore viral infections. Dilating drops for pain. Surgery through keratoplasty or keratectomy if unresponsive. Each type of infectious keratitis can be vision threatening and lead to corneal transplant and permanently reduced vision. Bacterial keratitis’ are usually the easiest to treat but also tend to progress the fastest and necessitate the earliest treatment. Fungal and protozoan keratitis tend to progress much slower and are more difficult to treat leading to higher odds of needing surgical intervention. Viral keratitis is often recurrent and can be triggered by UV, trauma, and stress but rarely leads to permanent vision loss.
- Herpes Zoster Ophthalmicus
Dr Ben Wild The contents of the orbits of the skull include many tissues such as the optic nerves, extensions of the trigeminal nerves, orbital fat, eye muscles, the lacrimal glands, the eyes themselves, and much more. A frontal view of a healthy eye. Herpes zoster ophthalmicus (HZO), aka shingles involving the eye, refers to when the zoster virus (same as the chickenpox virus) exits the trigeminal nerve and infects the tissues of the orbit and the skin on half of the face. The skin rash covers exactly either the right or left side of the face and is a tell-tale sign when it comes to shingles. If the rash extends to the tip of the nose there is a much higher chance the virus will also affect the eye and cause conjunctivitis, keratitis, vasculitis, episcleritis, scleritis, uveitis, neuritis, nerve palsies, neuralgia, neurotrophic ulcers or others. It usually occurs in the 6th and/or 7th decade of life and becomes more severe in immunodeficient people. Front view of an eye with HZO including a skin rash, conjunctivitis and keratitis. Shingles usually has a fairly sudden onset and presents alongside tiredness, fever, feeling unwell, and itching, tingling, and burning of the skin. Signs Rash covering either left or right of the face, eyelid swelling, and red eye. Symptoms Eye pain, light sensitivity, burred vision. Causes Varicella zoster virus infection. Risk Factors Stress. Prevention Childhood infection with chickenpox and receive the varicella zoster vaccine (prevents infection in 82% of cases and 100% of severe cases). Treatments Treatment starts with either acyclovir, famciclovir, or valacyclovir anti-viral pills, ideally within the first 3 days, followed by other add-ons depending on which tissue is affected. · Conjunctivitis: artificial tears and cold compresses for comfort. · Keratitis: artificial tears and steroid drops. · Episcleritis: non-steroidal anti-inflammatory drops. · Scleritis, vasculitis, neuritis: steroid pills. · Uveitis: steroid pills or drops. · Nerve palsies and neuralgias: no treatment. Mild to moderate HZO is usually easily treatable with the facial rash lasting a week or two. Full recovery from mild to moderate cases is likely. Severe cases of HZO can cause permanent corneal scarring, nerve damage, permanent neuralgia pain, cataracts, glaucoma, retinal scarring and in worst case scenarios, can lead to removal of the eye.
- Thyroid Eye Disease/Grave's Disease
Dr Ben Wild Thyroid eye disease (TED), aka Grave’s disease, refers to a condition where, instead of the thyroid gland being stimulated by thyroid stimulating hormone from the pituitary gland in the brain, it reacts to destructive antibodies created by the immune system. In TED, these antibodies can also attach to ocular tissues such as orbital fat, lacrimal glands, and eye muscles. This can cause swelling of these tissues up to 8x their normal size. This is usually seen in women in their 4th to 5th decade of life who smoke and is accompanied by weight loss despite healthy appetite, increased bowel movements, nervousness, irritability, palpations, and/or weakness and fatigue. A frontal view of a healthy eye. There are 2 stages of TED. Stage 1 refers to the inflammatory stage where the antibodies attack orbital tissues and cause swelling. This stage is accompanied by pain, swelling of the eye, bulging of one or both eyes, loss of vision, double vision, and more. Stage 2 refers to the fibrotic (scarring) stage. The eye is no longer inflamed, is usually clear and painless, but the scarring usually results in restricted eye movements and double vision. Frontal view of an eye with active severe thyroid eye disease. Thyroid dysfunction can be diagnosed after blood work showing elevated T3/T4 (thyroid) levels yet low TSH levels. TED is diagnosed after thyroid dysfunction has been discovered and MRI/CT scans of the orbits show swelling of orbital tissue. Signs Red eyes, swollen eyes, swollen lids, bulging eyes, eyelid retraction, difficulty closing eyes. Symptoms Pain, loss of vision, double vision, grittiness, tearing, light sensitivity. Causes Autoimmune disorder (Grave’s disease). Risk Factors Smoking. Prevention Have routine physicals with lab work by your family doctor, discontinue smoking, and seek treatment if thyroid levels are elevated. Treatments TED is a vision threatening condition. If the orbital tissue swells too much, it will compress the optic nerve and cause permanent blind spots. It can also result in the cornea failing, resulting in scarring and, again, vision loss. Additionally, it can cause potentially permanent bulging eyes (proptosis) and double vision. Prompt diagnosis and treatment can drastically lower the likelihood of vision loss.
- Retention/Inclusion Cyst and Lymphangiectasia
Dr Ben Wild The conjunctiva is a clear layer of tissue that extends from the edge of the cornea, around the visible portion of the eye in front of the white sclera, and even covers the back surface of the eyelids. It posses as a barrier against foreign material contributes to the tear film. A frontal view of a healthy eye. Retention (or inclusion) cysts and lymphangiectasias represent thinly walled lesions over the white part of the eye (sclera), containing either clear or semi-clear fluid. Theses cysts can be bilateral (both eyes) or unilateral (one eye) and do not often cause any discomfort. A sagittal view of an eye with a retention cyst. Retention cysts represent very common single entities of fluid build up under the conjunctiva whereas lymphangiectasias, which can be single cysts, tend to be sausage-link like channels of cysts. They are much less common and thought to be a build up of fluid from blocked lymphatic channels. Both of these tend to resolve spontaneously but can remain chronic. Signs Clear/semi-clear fluid filled cyst over the white parts of the eye. Symptoms Usually none but sometimes minor irritation and foreign body sensation. Causes Usually idiopathic (no cause). Risk Factors Ocular inflammation, allergies, and/or trauma. Prevention There are no known preventative measures. Treatments · Artificial tears for discomfort since they can resolve on their own. · Puncture with needle (tend to recur). · Cyst wall excision (tend not to recur). Neither of these conditions are vision threatening and represent only minor inconveniences to day-to-day life. They tend to be seen as cosmetic blemishes rather than true ocular conditions.
- Neurotrophic Keratopathy
Dr Ben Wild The cornea is the outermost layer of the eye in front of the iris. It is a clear tissue, void of any blood vessels, and is one of the main optical components responsible focusing lights on the retina. The cornea is composed of 5 different layers with the 3 main layers being the epithelium (outermost layer), stroma (providing the focusing power and strength of the cornea) and the endothelium (innermost layer responsible for making sure the cornea doesn’t swell). A frontal view of a healthy eye (left) and an eye with a whitish/grey neurotrophic ulcer (right). Interestingly, the entire corneal epithelium gets replaced every 10 days, allowing the cornea to heal itself very quickly. This rapid healing process is largely due to the release of growth factors from corneal nerves that filter through the stroma and into the epithelium. Without growth signals from these nerves the cornea will not heal. A sagittal view of a healthy cornea (left) and a cornea with a neurotrophic ulcer (right). Neurotrophic keratopathy occurs due to a variety of conditions where the corneal nerves stop functioning. Without these nerve signals, the epithelium cannot regenerate. This leads to the development of an ulcer. Because the epithelium cannot fully heal, bacterial and fungal infections are more common. Unlike most other ulcers, these ulcers do not typically cause pain, because the nerves that produce pain signals are not functioning. Signs Non-healing white/grey spot on the cornea, possible red eye. Symptoms Blurry vision, slight irritation, numb eye. Causes Loss of nerve fiber stimulation of the corneal epithelium. Risk Factors Drug toxicity, diabetes, herpes simplex virus (cold sore), herpes zoster (shingles), tumours, facial surgeries, refractive laser eye surgeries, other eye surgeries, stroke, various neuralgias. Prevention Avoid use of anesthetic eye drops and seek early treatment of herpes zoster or simplex in the eye. Treatments · Bandage contact lens. · Preservative free artificial tears ever hour or 2. · Tetracycline pills. · Tape lids shut at night. · Amniotic membrane implantation. · Tarsorrhaphy (sow eyelid shut for an extended period of time). Mild neurotrophic keratopathy is an easily manageable condition that can usually be successfully treated with either a bandage contact lens or preservative free artificial tears. Severe keratopathy can lead to melting and perforation of the cornea and possible removal of the eye. Usually, amniotic membrane implantation and/or tarsorrhaphy can avert eye removal but at the severe stage, full recovery is usually not possible.
- Spasms of the Eye
Dr Ben Wild The eyelids are full of muscles. From the orbicularis muscles that circulate the eyes, to the levator muscles that pull the upper eyelids upwards, to the tarsal muscles that provide protection and help raise the upper eyelids. The orbicularis is controlled by the facial nerve, the levator is controlled by the oculomotor nerve and the tarsal muscles are controlled by the sympathetic nervous system. Spasms occur when these nerves, without a known stimulus, cause contraction of the muscles they control. Myokemia is the most common spasm that affects eyelids. It can affect either the top or bottom lids but usually only one at a time. These spasms can be very short lasting or go on for weeks and be barely noticeable to very bothersome. Essential blepharospasms are uncommon, usually without a known cause, and can progress to involuntary bilateral (both sides of the face) orbicularis spasms that may affect other muscles on the face controlled by the facial nerve. Reflex blepharospasms are spasms created by bright light, ocular surface disease like severe dry eye, and extrapyramidal diseases like Parkinson’s and necessitates a central and peripheral nervous system assessment. Hemifacial spasms start at the orbicularis muscle and then spreads to the other facial muscles on one side of the face. Neuroimaging may or may not be needed. Signs Symptoms Causes Over stimulated oculomotor nerve or facial nerve usually of an unknown cause. Risk factors Prevention Journal when the eye spasms occur and try to determine the trigger. Treatments: there are no known treatments but the episodes can be managed. Episodes of myokemia can be short lived or last many weeks and can come and go randomly. It is not uncommon to be affected with multiple episodes over a period of months but then have the issue resolve and never reccur. The episodes do not cause any damage and therefore there are no known long-term complications. Essential, reflex and hemifacial spasms may require neuroimaging and nervous system testing. The spasms themselves do not cause damage but the underlying conditions, if not treated appropriately, may worsen.
- Marginal Keratitis
Dr Ben Wild The eyelids are made up of various types of skin, muscle, glands, hair follicles and much more. Their purpose is to protect the eyes from dryness, bright lights and irritants. As with skin everywhere on the body, the eyelid skin harbors bacteria. If the wrong type of bacteria colonize the eyelids or if there is an overgrowth of the normal bacteria, the eyelids can cause harm to the eyes. This harm can involve the cornea, the clear outermost layer of the eye in front of the colored iris, and the conjunctiva, the clear layer over the white part of the eye otherwise know as the sclera. Frontal view of a healthy eye. Marginal keratitis refers to a hypersentivity reaction within the cornea to the bacteria on the eyelids and is seen as white dots, representing colonies of white blood cells, around the edge of the cornea in red eyes. If left untreated, these white blood cells can cause scarring, ulceration, and/or blood vessel growth into the cornea. It is usually associated with blepharitis and/or rosacea. Frontal view of a an eye with marginal keratitis. Signs White dots around the edge of the cornea in a red eye. Symptoms Mild to moderate discomfort, redness, tearing. Causes Allergic hypersensitivity reaction to toxins created by the bacteria on the eyelids. Risk factors Blepharitis, rosacea, eczema. Prevention Daily eyelid hygiene. Treatments · Antibiotic eye drops and ointment. · Steroid eye drops. · Oral tetracycline pills. Most cases of marginal keratitis are very easily managed through the aforementioned treatments. Without treatment, marginal keratitis can resolve on its own but is much more likely to cause permanent scarring, ulceration, blood vessel growth into the cornea. The causes of these conditions can usually be managed with proper lid hygiene but in some cases, need continuous treatment.