What is the Canal of Schlemm? (with pictures) What is the Canal of Schlemm? Last Modified Date: 19 December 2016 Copyright Protected: Top 10 unbelievable historical concurrencies The Canal of Schlemm is a canal located in the eye, also known as the scleral venous sinus or Schlemm's canal. Circular in shape, the canal's function is to collect fluid called aqueous humor from the anterior chamber of the eye and move it to the blood and vascular system. The aqueous humor is moved via the anterior ciliary veins. Much like a lymphatic vessel, with endothelium lining, the canal also is covered by a mesh-like substance referred to as trabecular meshwork. This sinus received its name from noted German anatomist Friedrich Schlemm. The aqueous humor plays a major role in the function of the canal of Schlemm as well as in the function of the human eye itself. This substance is produced by secretory epithelium or skin tissue, that lines the ciliary processes and is then released into the posterior chamber of the eye where it helps regulate intraocular pressure between the anterior and posterior portions.

The aqueous humor is also present in the anterior portion of the eye, and its job is to mesh with a huge number of collagen fibrils and drain through the duct or canal of Schlemm. The excess aqueous humor fluid is then released into the lymphatic system and allowed to be carried out into the general lymph circulation of the body. Both Schlemm's canal and the aqueous humor are vital to the health and function of the eye. It is critical for the posterior and anterior portions of the eye to maintain a careful balance of aqueous humor production and drainage to ensure proper pressure of two chambers. The balance of production and drainage also serves to promote the correct spatial distances between the various organelles of the eye. If this important balance is not maintained, it is common for eye disorders relating to distortion of the size and shape of the eyeball to present, and there is an increased potential for seriously impaired vision to occur. There are two ways in which the canal of Schlemm can be adversely affected, causing dysfunction and possible damage. In addition to eye disease, physical injury to the area can also create an imbalance of the aqueous humor and damage the scleral venous sinus.

If too much aqueous humor is produced, the intraocular pressure is likely to rise, causing the potential for serious eye diseases , such as glaucoma . This disease is characterized by optic nerve atrophy, impaired, blurry vision , and eye retina detachment. Left untreated, glaucoma can also result in permanent vision loss. Ad Glaucoma - body, causes, How Does Glaucoma Affect the Eye? Glaucoma Glaucoma Photo by: LightScribe Glaucoma (glaw-KO-ma) is a group of disorders that cause fluid pressure to rise inside the eye, which may result in vision loss. KEYWORDS for searching the Internet and other reference sources Ophthalmology Vision If a balloon is slowly filled with water, eventually it will burst. But if the same balloon has several pin-sized holes at one end, then it becomes possible to continue adding water to the balloon to maintain its round shape, without breaking the balloon, as long as the amount of water being added is equal to the amount escaping through the pinholes. The eye has a similar system of liquid that continuously flows in and out of a small chamber at the front of the eyeball.

The problem for people with glaucoma is that the drainage out of the eye is blocked or not working properly. It is similar to the balloon that is filling with water. Without a way to make room for more liquid, pressure builds up. Although a pressure buildup will not cause the eye to burst, it may damage nerves at the rear of the eyeball that carry images to the brain. Glaucoma is one of the leading causes of blindness in the United States. It affects more than 3 million people, especially the elderly and people of African ancestry. The disease also is one of the sneakiest eye disorders. Pressure can grow in the eye for years before the effects on vision are noticed. By then, often the damage has been done. Anatomy of the eye. The arrows show the flow of aqueous humor from behind the iris, through the pupil, to the front of the eye, where it drains through the canal of Schlemm. How Does Glaucoma Affect the Eye? The eye is about the same size as a ping-pong ball and is divided into two compartments.

The larger compartment at the rear of the eye contains a gel-like substance called vitreous (VIT-re-us) humor, which helps to maintain the eyeball's shape and to transmit light. The front compartment, or anterior chamber, is smaller and is filled with a watery liquid called aqueous (AY-kwee-us) humor. This clear liquid brings in nutrients vital to the eye's health and carries out waste that can damage it. The aqueous humor flows from behind the front colored portion of the eye, which is called the iris. It moves through the pupil, the opening in the center of the iris, into the front chamber of the eye. The liquid flows through the chamber and out a tiny drainage canal that has a fine, mesh-like covering. The small hole on the canal rests at an angle where the colored iris meets the cornea, the clear cup-shaped disc at the front of the eyeball. About 90 to 95 percent of people with glaucoma have a problem with this drainage system. The cause is unknown, as there is no visible blockage. It appears that the cells in the mesh covering the drainage canal do not do their job properly, or lose their ability to allow proper drainage over time.

Glaucoma develops gradually, but there is a rarer acute * form of glaucoma that develops suddenly when the iris closes off the drainage canal. This causes a painful medical emergency that requires immediate treatment. The cause of most cases of glaucoma is not understood, although people of African ancestry, people who have diabetes or other family members with glaucoma, or those who have suffered eye injuries are at greater risk. Aging is another risk factor for glaucoma. How Is Glaucoma Diagnosed? Except for the rare cases of acute glaucoma that develop suddenly, most people do not realize they have glaucoma. As pressure is building in the eye, many of the millions of nerve cells at the rear of the eye are destroyed. The nerves that die first affect peripheral (pe-RIF-er-al) vision, or how well people see out of the sides of the eyes. When the loss of vision becomes severe enough for a person to notice, the damage is so great that little can be done. The best way to diagnose glaucoma is through an eye exam that uses an instrument called a tonometer (to-NOM-e-ter) to measure the pressure in the eye.

One type of tonometer registers eye pressure by lightly touching the eye's surface. Eyedrops are used to make this procedure painless. Another tonometer uses a puff of air to measure eye pressure. The doctor or eye specialist (ophthalmologist or optometrist) also may use a scope that shines light in the eye to look for damage to the optic nerve. Peripheral vision can be checked as part of the eye exam. * acute means sudden, short, and severe. Why Are Early Diagnosis and Treatment Important? Diagnosis Early diagnosis of glaucoma is the key to preventing vision loss. If glaucoma is discovered before the increased eye pressure has destroyed many nerves, vision can be saved in many cases. Routine eye exams, including tests for glaucoma, are important, especially as adults pass age 35. Such eye exams are especially important for people at greatest risk for glaucoma, including people of African ancestry, people with relatives who have glaucoma, people with diabetes, and people with previous eye injuries. Treatment The most common treatment involves eyedrops that reduce pressure. Sometimes surgery is necessary either to open the drainage canal or to create a new one.

No Mountain Too High Glaucoma rarely occurs in young people, but Erik Weilenmayer was born with an eye disease that caused glaucoma. By age 13, he was totally blind. Erik did not let glaucoma prevent him from becoming a teacher and a mountain climber. He has scaled some of the toughest peaks, including Alaska's Mt. McKinley, the highest in the United States. "When I first went blind, I wondered what I could do," Weilenmayer said in 1998. "It's really a kick to do extreme activities and do them well—and no more dangerously than anyone else." Erik's accomplishments are a reminder that physical challenges and differences do not have to prevent people from participating in life's most difficult and demanding activities. See also Introduction to Glaucoma | Glaucoma Flashcards Glaucoma is a disease where the optic nerve dies. We are not sure why or how this happens (there are many mechanical, vascular, and biochemical theories) but high intraocular pressure certainly seems to be associated, if not entirely the cause, of optic nerve death.

Glaucoma is one of the leading causes of preventable blindness in the U.S., and patients with acute glaucoma can develop irreversible vision loss within a few hours, so it is important that you understand how this disease works and recognize it in your patients. The Aqueous Pathway Before continuing we should review the pathway of aqueous humor flow. Aqueous is the fluid that fills the front part of the eye, and it is important for maintaining the shape of the eye and providing nourishment for the avascular lens and cornea. Aqueous humor is first produced by the ciliary body within the posterior chamber. After filling the posterior chamber, aqueous moves forward around the lens and flows through the pupil into the anterior chamber. As the anterior chamber fills, the aqueous spreads outwards into the angle formed by the iris and cornea. Within this irido-corneal angle the aqueous exits the eye by filtering through the trabecular meshwork into the Canal of Schlemm, where it returns back into the blood circulation. The pressure within the eye is maintained by this steady state of aqueous production and egress, and it is an imbalance in this equilibrium that causes the increase pressure associated with glaucoma. Open vs.

Closed-Angle Glaucoma There are two categories of glaucoma and they have very different mechanisms. Open-angle glaucoma is the most common type in our country. It occurs from decreased aqueous drainage caused by an unidentified dysfunction or microscopic clogging of the trabecular meshwork. This leads to chronically elevated eye pressure, and over many years, gradual vision loss. This differs from closed-angle glaucoma, also called “acute glaucoma,” which occurs when the angle between the cornea and iris closes abruptly. With this closure, aqueous fluid can’t access the drainage pathway entirely, causing ocular pressure to increase rapidly. This is an ophthalmological emergency and patients can lose all vision in their eye within hours. Let’s examine each of these types of glaucoma in more detail. Open-Angle Glaucoma The majority of glaucoma patients (about 80% ) have chronic open angle glaucoma. Most patients are over the age of 40. This condition is more common in African Americans, and has a strong familial inheritance. The major risk factors are family history, age, race, high eye pressure, and large vertical nerve cupping.

More recently, thin-corneas have been found to be a major risk factor, though this mechanism is not well understood. The underlying mechanism for open-angle glaucoma involves degeneration of the trabecular meshwork filter, usually by unknown causes, that leads to aqueous backup and chronically elevated eye pressure. With prolonged high pressure, the ganglion nerves in the retina (the same nerves that form the optic nerve) atrophy. The exact mechanism for this nerve damage is poorly understood and proposed mechanisms include stretching, vascular compromise, and glutamate transmitter pathways. As the ganglion nerves are progressively destroyed, vision is gradually lost. Open-angle glaucoma has the reputation of being the “sneaky thief of sight” because the visual loss occurs so slowly that many patients don’t realize they have the disease until it is far advanced. Because the disease is otherwise asymptomatic, detecting open-angle glaucoma requires early pressure screening. Free screening clinics also use different types of automated visual-field testing to detect subtle peripheral vision loss. Presentation Open-angle glaucoma patients usually present with three exam findings: elevated eye pressures, optic disk changes, and repeatable visual field loss patterns. 1.

Pressure: The most accurate way to measure eye pressure is with the Goldman applanation tonometer. This is a device mounted on the slit-lamp that measures the force required to flatten a fixed area of the cornea. Normal pressures range from 10 to 22 mm Hg, while glaucoma patients can measure over 22 mm Hg. Keep in mind that eye pressure can fluctuate throughout the day (typically highest in the morning) so the pressure should be checked with each visit and the time of measurement should be noted. Also, some glaucomatous eyes have a “normal” pressure. In other words, a “good pressure” doesn’t rule out glaucoma, nor does a high pressure necessarily indicate glaucoma. You can also measure pressure with a device called a “Tono-Pen.” This expensive little device is handy for bed-bound patients and down in the emergency room, though it’s inaccurate in the wrong hands! Corneal Thickness can affect your pressure measurement: When we measure the pressure in the eye, we are actually measuring how much resistance we get when pressing on the cornea.

This is analogous to kicking a car-tire with your foot or pressing your hand against a bicycle tire to estimate how much air pressure is inside. We do the same thing with the Goldman applanation tonometer mounted on the slit-lamp – we measure how much force it takes to flatten a 3mm diameter area of corneal surface. The pressure measurements on the Goldman were calibrated using an average corneal thickness of approximately 540nm. However, some patients have very thin or thick corneas. I like to describe these as “thin bicycle” or “thick truck-tire” corneas. When you press on a thick cornea (a truck-tire cornea) the pressure will seem higher than it really is! This makes sense … if you kick a flat truck-tire, it will still hurt your foot because that rubber is so darn thick. The opposite is true for thin corneas – they feel squishy no matter how much air pressure. This thickness variability is important in glaucoma clinic so we can calibrate the accuracy of our pressure readings. This is why we always check corneal thickness with an ultrasonic pachymeter on the first visit. 2.

Fundus Exam: The optic disk looks striking in advanced glaucoma. In normal patients, the optic disk has a physiological indentation or “cup” that is less than one-third the disk diameter. With glaucoma, the ganglion nerve layer slowly dies away, and, as fewer ganglion nerves course through the optic disk, the amount of cupping increases. A cup to disk ratio greater than 0.5 or an asymmetry between the eyes suggests ganglion atrophy caused by glaucoma. The ISNT Rule When you look at your patient’s optic nerve, you’ll notice that the cup doesn’t sit directly in the middle of the disk. The cup is slightly off-center – this makes sense as the optic nerve enters the back of the eyeball at an angle. The space between the inner cup and surrounding disk is called the neural rim and is comprised of the actual retinal ganglion nerves. In a normal eye, this rim follows the ISNT rule of decreasing thickness … meaning that the Inferior rim is thickest while the Temporal rim is the skinniest. With glaucoma, you often see vertical thinning and notching of the inferior and superior rims.

This deviation from the ISNT rule is another clue that glaucoma might be killing off the nerve. You can also see undermining of the rim (like in the right drawing) where the blood vessels dive out of view under the rim edge. 3. Visual Loss: The vision loss from chronic glaucoma occurs in characteristic patterns that can be followed by automated perimetry (machines that map out the peripheral vision). The central vision is typically spared – in fact, late stage patients may have 20/20 central vision, but be otherwise legally blind because of peripheral blindness. FUN FACT! The giant squid has the largest eyeball in the world. This enormous deep-sea predator can weigh up to 2.5 tons and 55 feet in length. Its eye can be a more than a foot in diameter! Wow! Treatment: Since IOP is the only risk factor we can treat, the primary treatment of glaucoma focuses on decreasing eye pressure to less than 20 mm Hg or even lower depending upon the severity of disease. Treatment may be either medical or surgical. Medical Treatment Topical beta-blockers are the traditional therapy for these patients and have been around for decades.

Beta-blockers work by decreasing aqueous humor production at the ciliary body. Unfortunately, systemic side effects can occur from nasal absorption, making it especially important to ask your patients about history of asthma, COPD, and cardiac problems. These days, many physicians are using newer drugs like topical CAIs, alpha-agonists, and prostaglandin analogues for first-line therapy, as they have fewer systemic side effects. Prostaglandin analogues like latanoprost (Xalatan™) are the newest of these glaucoma drugs, and they are very popular as a first-line agent. They work by increasing aqueous humor outflow. They do have some side effects, though. They can make eyelashes grow longer (many patients actually like this), and in a few patients may darken the iris color, turning green and blue eyes brown. Surgical Treatment for Chronic Glaucoma If eyedrops aren’t working, there are several surgical techniques available to relieve eye pressure. One common surgery is the trabeculectomy, where an alternate drainage pathway is surgically created. A small hole is cut through the superior limbus, creating a drainage tract from the anterior chamber to a space under the conjunctiva.

This can be very effective in decreasing pressure, but if the patient is a rapid healer the shunt can scar down and close, so anti-metabolites like mitomycin-C are often applied to the site. If this surgery doesn’t work, a plastic tube-shunt can be inserted into the anterior chamber that drains to a plate fixed under the conjunctiva further back. Several laser procedures can also help. Argon laser trabeculoplasty (ALT) can be used to burn portions of the trabecular meshwork itself. The resulting scarring opens up the meshwork and increases outflow. A laser can also be used to burn the ciliary body to decrease aqueous production at its source. Acute Glaucoma Acute glaucoma is a medical emergency. The most common mechanism is pupillary block. This occurs when the lens plasters up against the back of the iris, blocking aqueous flow through the pupil. This resistance produces a pressure gradient (this is a good buzz word to memorize) across the iris that forces the iris and lens to move anteriorly. When the iris moves forward, the irido-corneal angle closes, blocking the trabecular meshwork.

Without an exit pathway, aqueous fluid builds up, eye pressure increases rapidly, and the retina is damaged from stretching and decreased blood supply. The outflow angle can close for many reasons, and people with naturally shallow anterior chambers such as hyperopes (far-sighted people with small eyes) and Asians are predisposed to developing angle closure. One inciting condition that is typical in acute glaucoma is pupil dilation — many patients describe onset of their symptoms occurring while in the dark or during stressful situations. When the iris dilates, the iris muscle gets thicker and the irido-corneal angle becomes smaller, making it more likely to spontaneously close. Along those lines, medications that dilate the eye, such as over-the-counter antihistamines and cold medications, also predispose angle closure. Presentation These patients will present with an extremely red and painful eye, often complaining of nausea and vomiting. On exam, you’ll find their pupil sluggish and mid-dilated. Pressures in the affected eye can be very high, often 60 mm Hg or higher. The eye will feel rock hard, and you can actually palpate the difference between the eyes with your fingers. One classic sign that patients often describe is seeing halos around lights.

This occurs because the cornea swells as water is pushed under high pressure through the endothelium into the corneal stroma. This corneal swelling also makes it hard for you to see into the eye, further complicating diagnosis and treatment. Acute Glaucoma Exam Techniques: Ophthalmologic examination for acute glaucoma involves measuring the eye pressure, accessing the anterior chamber angle, and a fundus exam. One trick to determine whether an angle is shallow is to shine a simple penlight across the eyes. If the iris is pushed forward, it will cast a shadow. Additionally, an ophthalmologist can visualize the angle directly through gonioscopy. Here’s how it works: Gonioscopy: Normally, the inside angle cannot be seen with a microscope because the cornea-air interface creates “total internal reflection.” However, we can use a goniolens, which is a special glass lens with mirrors on its sides, to look directly at the angle. When the glass lens is placed directly onto the cornea, the cornea-air interface reflection is broken and light from the angle can escape and be seen through the mirrors. We can see the concept of “total internal reflection” in nature.

For example, if you’ve ever gone snorkeling in water, you may notice that the water’s surface above you looks like a mirror. The flying fish uses this phenomenon to escape from predators. When attacked, the flying fish leaps from the water and glides above the surface so the shark can’t see them – effectively disappearing. This is also how fiber optic cables work, with light bouncing off the walls of the cable. Acute Glaucoma Treatment In cases of acute glaucoma, you want to decrease the pressure in the eye as quickly as possible. A “kitchen sink” approach is often used, throwing many treatments on at once. You can decrease aqueous production using a topical beta-blocker like Timolol and a carbonic anhydrase inhibitor like Diamox. Also, osmotic agents such as oral glycerin or IV mannitol (even ethanol, in a bind) can be given systemically to draw fluid out of the eye and back into the bloodstream. Finally, a miotic such as pilocarpine may be helpful in certain cases to constrict the pupil and thus open up the outflow angle. You can also use topical glycerin to transiently dehydrate/clear the cornea to aid with examination.

Ultimately, these patients need surgical treatment to avoid recurrence of their angle closure. A high intensity laser can burn a hole through the iris and create a communication between the posterior and anterior chambers, relieving the pressure gradient (buzzword!!) across the iris, and allowing it to move back into a normal position. This opens up the trabecular meshwork and allows aqueous fluid to flow freely out of the eye. This procedure is typically performed on both eyes because these patients are predisposed to having attacks in the other eye as well. Other types of glaucoma 1. Neovascular Glaucoma: This can occur in diabetic patients or those with a retinal vein occlusion. VEGF production from areas of ischemic retina can float forward through the pupil and promote neovascularization of the iris. In the early stages, a fibrous membrane forms on the iris-cornea angle that blocks outflow and forms an open-angle glaucoma. At later stages of neovascularization, the new vessels actually pull the iris forward and cause a closed angle glaucoma that is essentially irreversible. You treat this by lasering the peripheral retina to decrease the angiogenic VEGF production and decrease the rate of neovascularization.

Neovascular glaucoma is very hard to treat and most of these patients end up needing a surgical intervention like a tube-shunt. 2. Pigment Dispersion Syndrome (PDS): Occurs when the pigmented back-surface of the iris rubs against the radial zonules supporting the lens. Little flecks of pigment are shed into the aqueous and end up clogging the trabecular meshwork drain. This process usually occurs in young white males with myopic eyes. They suffer from attacks of high pressure after exercise when pigment gets rubbed off the iris. You can see this pigment in the trabecular meshwork on gonioscopy, and even find trans-illumination defects of the iris at the slit-lamp. Some of the pigment will stick to the inner-corneal surface, and because of convection currents in the aqueous, form a vertical line of pigment on the inner corneal surface called a Krukenberg spindle. 3. Pseudoexfoliation Syndrome (PXF) In this systemic condition, basement membrane-like material is deposited throughout the body. This material adheres to the anterior lens capsule, creating a rough surface.

As the overlying iris dilates and contracts with daily activity, pigment is rubbed off and clogs the trabecular drain. These patients also suffer from zonular instability, making cataract operations difficult. Summary That is glaucoma in a nutshell. Chronic, open-angle glaucoma is very common (in this country) and leads to gradual visual loss, while acute closed-angle glaucoma is infrequent but an emergency that needs urgent treatment to avoid blindness. Pimp Questions 1. What is glaucoma? What actually causes damage to the neurons and optic nerve with glaucoma? Nobody is sure exactly “what glaucoma is” but at its most basic, glaucoma is gradual death of the optic nerve. If an attending asks you this question, say “knowbody knows” or “death of the optic nerve.” If you say “high pressure” you’ll be laughed at (glaucoma specialists are odd ducks). The optic nerve damage arises from pressure, stretching, sheer forces, vascular compromise, or some kind of hormone regulator – we’re not sure of the mechanism. 2. What is the flow-pathway for aqueous fluid? Where is it made, and where does it leave the eye?

Aqueous is first produced by the ciliary body. It then flows forward through the pupil into the anterior chamber. Finally, aqueous drains through the trabecular meshwork and back into the venous system via the canal of Schlemm. 3. What’s the difference between open-angle and closed-angle glaucoma? How about chronic versus acute glaucoma? Open angle is a common, chronic condition where aqueous drainage is impaired. Closed-angle glaucoma is caused by acute closure of the irido-corneal angle leading to blockage of ALL aqueous drainage – an ophthalmologic emergency that can quickly lead to blindness. 4. What are the risk factors for developing primary open-angle glaucoma? This is an important list and since I glossed over them in the chapter, here they are again: High intraocular pressure (obviously) Race (African American and Hispanics) Suspicious optic nerve appearance (large vertical cupping) Thin central corneal thickness (** remember this one!) There are other possible risk factors, but I’d focus on those above.

These risk factors explain why we always ask our patients about familial history and why we check pachymetry (corneal thickness by ultrasound) on the first glaucoma visit. 5. What do we measure to monitor and follow progression in glaucoma patients? We generally check three things: pressure, disk changes by 3D photograph, and visual fields. Good stereo slides are difficult to obtain, so many use other imaging modalities like HRT or OCT. 6. What does corneal thickness have to do with glaucoma (as far as risk for developing glaucoma)? The OHTS trial showed that people with thin corneas are at higher risk for glaucoma, independent of other risk factors. We’re not sure why, but it’s believed that people with thin corneas are anatomically predisposed to optic nerve damage. We measure corneal thickness with a small ultrasound probe (this is called pachymetry) with all new glaucoma patients. 7. What’s a normal eye pressure? Does a patient with pressure of 14 have glaucoma? About 10 to 22.

While glaucoma is classically associated with high pressure, there is a significant minority of patients with glaucoma with normal pressure. Also, pressure fluctuates throughout the day and we typically write down the time in the notes. Some studies have noted higher rates of glaucoma in people with large diurnal shifts in eye-pressure. This observation could be compared to diabetic suspects with large diurnal shifts in random-glucose measurements. 8. A glaucoma suspect is found on first visit to have a pressure of 19. Her corneal thickness, however, measures only 450nm. Do you think her actual eye pressure is HIGHER or LOWER than 19? Definitely higher. This patient has thin “bicycle-tire corneas” that “feel soft” when measured by the Goldman applanation. This woman’s actual pressure is probably well over 22, increasing her risk for glaucomatous damage progression. 9. What kind of vision loss occurs with glaucoma? Typically loss of eyesight occurs in the periphery first where the loss is less noticeable. Scotomas (visual field loss areas) in glaucoma tend to follow certain patterns that start in the mid-periphery.

Many patients don’t notice visual symptoms until the disease is far progressed. Generally, the central vision is spared until very late stages of glaucoma. 10. Why can’t you see the trabecular meshwork with the slit-lamp microscope? Because the trabecular drain is behind the limbus (around the corner) and we can’t see this area directly because of “total internal reflection” at the cornea-air interface. Gonioscopy allows direct visualization of the trabecular meshwork by interrupting the cornea-air interface with a glass lens. 11. What mechanisms do the glaucoma drops use to decrease pressure? Drops either decrease the amount of aqueous produced at the ciliary body or increase the aqueous outflow from the eye (generally via the uveal-scleral pathway or by direct trabecular meshwork outflow). 12. What retina findings do you see with glaucoma? You see increased cupping of the optic disk, usually in a vertical pattern that goes against the ISNT rule. You can sometimes see hemorrhages at the disk and undermining of the blood vessels as they exit the disk. 13. How can diabetes cause acute glaucoma?

Retinal ischemia can produce VEFG. As this molecule floats forward it can cause neovascularization of the iris, forming vascular membranes that cover the trabecular meshwork and clog the drainage angle. This leads to a severe neovascular glaucoma that is hard to manage. 14. You have a patient who appears to have a shallow anterior chambers and occludable angles. Would you use pilocarpine? In most cases, yes. Pilocarpine will constrict the pupils — by flattening the iris you potentially open up the drainage angle next to the trabecular meshwork. Pilocarpine will also decrease pressure in the eye by affecting aqueous production and egress. You probably wouldn’t use it long term in patients with occludable angles though, as pilo has a lot of side effects such as headache and blurry vision. Ultimately, anyone with occludable angles needs a laser peripheral iridotomy to equalize the pressure between anterior and posterior chambers. Canal - definition of canal by The Free Dictionary Canal - definition of canal by The Free Dictionary Related to canal: inguinal canal ca·nal 1. An artificial waterway or artificially improved river used for travel, shipping, or irrigation.

2. Anatomy A tube, duct, or passageway. 3. Astronomy One of the faint, hazy markings resembling straight lines on early telescopic images of the surface of Mars. tr.v. ca·nalled, ca·nal·ling, ca·nals or ca·naled or ca·nal·ing 1. To dig an artificial waterway through: canal an isthmus. 2. To provide with an artificial waterway or waterways. [Partly French, channel, and partly Middle English, tube (from Medieval Latin canāle), both from Latin canālis, tube, channel, probably from canna, small reed; see cane.] canal 1. (Civil Engineering) an artificial waterway constructed for navigation, irrigation, water power, etc 2. (Zoology) any of various tubular passages or ducts: the alimentary canal. 3. (Botany) any of various elongated intercellular spaces in plants 4. (Astronomy) astronomy any of the indistinct surface features of Mars originally thought to be a network of channels but not seen on close-range photographs.

They are caused by an optical illusion in which faint geological features appear to have a geometric structure vb (tr) , -nals, -nalling or -nalled, -nals, -naling or -naled 5. (Civil Engineering) to dig a canal through 6. to provide with a canal or canals [C15 (in the sense: pipe, tube): from Latin canālis channel, water pipe, from canna reed, cane1] ca•nal n., v. -nalled -naled, -nal•ling -nal•ing. n. 1. an artificial waterway for navigation, irrigation, etc. 2. a tubular passage for food, air, etc., in an animal or plant; duct. 3. channel; watercourse. 4. one of the long, dark lines on the planet Mars, as viewed from Earth. v.t. 5. to make a canal through. [1400–50; late Middle English: waterpipe, tubular passage < Latin canālis] canal - The holes in a sponge are called canals. See also related terms for holes .

canal I will have been canalling you will have been canalling he/she/it will have been canalling we will have been canalling you will have been canalling they will have been canalling Past Perfect Continuous Noun 1. canal - (astronomy) an indistinct surface feature of Mars once thought to be a system of channels; they are now believed to be an optical illusion astronomy , uranology - the branch of physics that studies celestial bodies and the universe as a whole channel - a deep and relatively narrow body of water (as in a river or a harbor or a strait linking two larger bodies) that allows the best passage for vessels; "the ship went aground in the channel" 2.

canal - a bodily passage or tube lined with epithelial cells and conveying a secretion or other substance; "the tear duct was obstructed"; "the alimentary canal"; "poison is released through a channel in the snake's fangs" duct , epithelial duct , channel pore - any small opening in the skin or outer surface of an animal passageway , passage - a path or channel or duct through or along which something may pass; "the nasal passages" ductule , ductulus - a very small duct canaliculus - a small canal or duct as in some bones and parts of plants canal of Schlemm , Schlemm's canal , sinus venosus sclerae - a circular canal in the eye that drains aqueous humor from the anterior chamber of the eye into the anterior ciliary veins venous sinus , sinus - a wide channel containing blood; does not have the coating of an ordinary blood vessel ampulla - the dilated portion of a canal or duct especially of the semicircular canals of the ear lachrymal duct , lacrimal duct , tear duct - any of several small ducts that carry tears from the lacrimal glands nasolacrimal duct - a duct that carries tears from the lacr

imal sac to the nasal cavity Haversian canal - any of the many tiny canals that contain blood vessels and connective tissue and that form a network in bone hepatic duct - the duct that drains bile from the liver canalis inguinalis , inguinal canal - oblique passage through the lower abdominal wall; in males it is the passage through which the testes descend into the scrotum and it contains the spermatic cord; in females it transmits the round ligament of the uterus bile duct , common bile duct - a duct formed by the hepatic and cystic ducts; opens into the duodenum pancreatic duct - a duct connecting the pancreas with the intestine lymph vessel , lymphatic vessel - a vascular duct that carries lymph which is eventually added to the venous blood circulation salivary duct - a duct through which saliva passes from the salivary gland into the mouth aqueductus cerebri , cerebral aqueduct , Sylvian aqueduct - a canal connecting the third and fourth ventricles ureter - either of a pair of thick-walled tubes that carry urine from the kidney to the urinary bladder urethra - duct through which urine is discharged in most mammals and which serves as the male genital duct canalis cerv

icis uteri , cervical canal - a spindle-shaped canal extending from the uterus to the vagina umbilical , umbilical cord - membranous duct connecting the fetus with the placenta vagina - the lower part of the female reproductive tract; a moist canal in female mammals extending from the labia minora to the uterus; "the vagina receives the penis during coitus"; "the vagina is elastic enough to allow the passage of a fetus" epididymis - a convoluted tubule in each testis; carries sperm to vas deferens ductus deferens , vas deferens - a duct that carries spermatozoa from the epididymis to the ejaculatory duct seminal duct - the efferent duct of the testis in man ejaculatory duct - a part of the seminal duct formed by the duct from the seminal vesicle and the vas deferens; passes through the prostate gland cartilaginous tube - a duct with cartilaginous walls bronchiole - any of the smallest bronchial ducts; ending in alveoli Young’s modulus of elasticity of Schlemm’s canal endothelial cells | SpringerLink , Volume 9, Issue 1 , pp 19–33 Young’s modulus of elasticity

 of Schlemm’s canal endothelial cells Authors 215 Downloads Abstract Schlemm’s canal (SC) endothelial cells are likely important in the physiology and pathophysiology of the aqueous drainage system of the eye, particularly in glaucoma.

The mechanical stiffness of these cells determines, in part, the extent to which they can support a pressure gradient and thus can be used to place limits on the flow resistance that this layer can generate in the eye. However, little is known about the biomechanical properties of SC endothelial cells. Our goal in this study was to estimate the effective Young’s modulus of elasticity of normal SC cells. To do so, we combined magnetic pulling cytometry of isolated cultured human SC cells with finite element modeling of the mechanical response of the cell to traction forces applied by adherent beads. Preliminary work showed that the immersion angles of beads attached to the SC cells had a major influence on bead response; therefore, we also measured bead immersion angle by confocal microscopy, using an empirical technique to correct for axial distortion of the confocal images. Our results showed that the upper bound for the effective Young’s modulus of elasticity of the cultured SC cells examined in this study, in central, non-nuclear regions, ranged between 1,007 and 3,053 Pa, which is similar to, although somewhat larger than values that have been measured for other endothelial cell types.

We compared these values to estimates of the modulus of primate SC cells in vivo, based on images of these cells under pressure loading, and found good agreement at low intraocular pressure (8–15 mm Hg). However, increasing intraocular pressure (22–30 mm Hg) appeared to cause a significant increase in the modulus of these cells. These moduli can be used to estimate the extent to which SC cells deform in response to the pressure drop across the inner wall endothelium and thereby estimate the extent to which they can generate outflow resistance. Keywords Magnetic bead pulling cytometryImmersion angleCell stiffnessGlaucoma References Allingham RR, de Kater AW, Ethier CR, Anderson PJ, Hertzmark E, Epstein DL (1992) The relationship between pore density and outflow facility in human eyes.

Invest Ophthalmol Vis Sci 33(5): 1661–1669 Google Scholar Alvarado JA, Alvarado RG, Yeh RF, Franse-Carman L, Marcellino GR, Brownstein MJ (2005) A new insight into the cellular regulation of aqueous outflow:how trabecular meshwork endothelial cells drive a mechanism that regulates the permeability of Schlemm’s canal endothelial cells. Br J Ophthalmol 89(11): 1500–1505. doi: 10.1136/bjo.2005.081307 CrossRef Google Scholar Bausch AR, Ziemann F, Boulbitch AA, Jacobson K, Sackmann E (1998) Local measurements of viscoelastic parameters of adherent cell surfaces by magnetic bead microrheometry. Biophys J 75(4): 2038–2049.

doi: 10.1016/S0006-3495(98)77646-5 CrossRef Google Scholar Bill A, Svedbergh B (1972) Scanning electron microscopic studies of the trabecular meshwork and the canal of Schlemm—an attempt to localize the main resistance to outflow of aqueous humor in man. Acta Ophthalmol (Copenh) 50: 295–320 CrossRef Google Scholar Braet F, Rotsch C, Wisse E, Radmacher M (1998) Comparison of fixed and living liver endothelial cells by atomic force microscopy. Appl Phys A Mater Sci Process 66: S575–S578 CrossRef Google Scholar Burke A, Roberts B, O’Brien E, Stamer W (2002) Effects of Na2EDTA and hydrostatic pressure on transendothelial electrical resistances and hydraulic conductivity of human Schlemm’s canal monolayers (in review) Caille N, Thoumine O, Tardy Y, Meister JJ (2002) Contribution of the nucleus to the mechanical properties of endothelial cells.

J Biomech 35(2): 177–187. doi: 10.1016/S0021-9290(01)00201-9 CrossRef Google Scholar Cheezum MK, Walker WF, Guilford WH (2001) Quantitative comparison of algorithms for tracking single fluorescent particles. Biophys J 81(4): 2378–2388. doi: 10.1016/S0006-3495(01)75884-5 CrossRef Google Scholar Costa KD, Sim AJ, Yin FC (2006) Non-Hertzian approach to analyzing mechanical properties of endothelial cells probed by atomic force microscopy. J Biomech Eng 128(2): 176–184. doi: 10.1115/1.2165690 CrossRef Google Scholar Deguchi S, Maeda K, Ohashi T, Sato M (2005) Flow-induced hardening of endothelial nucleus as an intracellular stress-bearing organelle.

J Biomech 38(9): 1751–1759. doi: 10.1016/j.jbiomech.2005.06.003 CrossRef Google Scholar Ethier C, Read A, Chan D (2004) Biomechanics of Schlemm’s canal endothelial cells:influence on F-actin architecture. Biophys J 87: 2828–2837. doi: 10.1529/biophysj.103.038133 CrossRef Google Scholar Ethier CR (2002) The inner wall of Schlemm’s canal (REVIEW). Exp Eye Res 74: 161–172. doi: 10.1006/exer.2002.1144 CrossRef Google Scholar Ethier CR, Simmons CA (2007) Introductory biomechanics: from cells to organisms.

Cambridge University Press, Cambridge Google Scholar Ethier CR, Zeng D, Read AT, Chan D, Gong H, Johnson M (2008) Pressure-induced deformation of Schlemm’s canal endothelial cells. ARVO, Ft. Lauderdale Google Scholar Feneberg W, Aepfelbacher M, Sackmann E (2004) Microviscoelasticity of the apical cell surface of human umbilical vein endothelial cells (HUVEC) within confluent monolayers. Biophys J 87(2): 1338–1350. doi: 10.1529/biophysj.103.037044 CrossRef Google Scholar Ferko MC, Patterson BW, Butler PJ (2006) High-resolution solid modeling of biological samples imaged with 3D fluorescence microscopy. Microsc Res Tech 69(8): 648–655. doi: 10.1002/jemt.20332 CrossRef Google Scholar Fung Y (1977) A first course in continuum mechanics.

Prentice-Hall Inc., Englewood Cliffs Google Scholar Gelles J, Schnapp B, Sheetz M (1988) Tracking kinesin-driven movements with nanometre-scale precision. Nature 331(4): 450–453. doi: 10.1038/331450a0 CrossRef Google Scholar Gilmont R (2002) Measurement and control liquid—viscosity correlations for flowmeter catculations. Chem Eng Prog 98(10): 36–41 Google Scholar Grierson I, Lee WR (1975) Pressure-induced changes in the ultrastructure of the endothelium lining Schlemm’s canal. Am J Ophthalmol 80: 863–884 Google Scholar Grierson I, Lee WR (1977) Light microscopic quantitaion of the endothelial vacuoles in Schlemm’s canal.

Am J Ophthalmol 84: 234–246 Google Scholar Henon S, Lenormand G, Richert A, Gallet F (1999) A new determination of the shear modulus of the human erythrocyte membrane using optical tweezers. Biophys J 76(2): 1145–1151. doi: 10.1016/S0006-3495(99)77279-6 CrossRef Google Scholar Hogan MJ, Alvarado JA, Weddel J (1971) Histology of the human eye: an atlas and textbook. W.B. Saunders Co., Philadelphia Google Scholar Humphrey J (2002) On mechanical modeling of dynamic changes in the structure and properties of adherent cells. Math Mech Solids 7: 521–539. doi: 10.1177/108128650200700504 MATH CrossRef MathSciNet Google Scholar Johnson M (2006) What controls aqueous humour outflow resistance?.

Exp Eye Res 82(4): 545–557. doi: 10.1016/j.exer.2005.10.011 CrossRef Google Scholar Johnson M, Chan D, Read T, Christensen C, Sit A, Ethier CR (2002) The pore density in the inner wall endothelium of Schlemm’s canal of glaucomatous eyes. Invest Ophthalmol Vis Sci 43: 2950–2955 Google Scholar Karcher H, Lammerding J, Huang H, Lee RT, Kamm RD, Kaazempur-Mofrad MR (2003) A three-dimensional viscoelastic model for cell deformation with experimental verification. Biophys J 85(5): 3336–3349.

doi: 10.1016/S0006-3495(03)74753-5 CrossRef Google Scholar Karl MO, Fleischhauer JC, Stamer WD, Peterson-Yantorno K, Mitchell CH, Stone RA, Civan MM (2005) Differential P1-purinergic modulation of human Schlemm’s canal inner-wall cells. Am J Physiol Cell Physiol 288(4): C784–C794. doi: 10.1152/ajpcell.00333.2004 CrossRef Google Scholar Kass MA, Heuer DK, Higginbotham EJ, Johnson CA, Keltner JL, Miller JP, Parrish RK 2nd, Wilson MR, Gordon MO (2002) The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol 120(6): 701–713. see comment.

discussion 829–30 Google Scholar Kataoka N, Iwaki K, Hashimoto K, Mochizuki S, Ogasawara Y, Sato M, Tsujioka K, Kajiya F (2002) Measurements of endothelial cell-to-cell and cell-to-substrate gaps and micromechanical properties of endothelial cells during monocyte adhesion. Proc Natl Acad Sci USA 99(24): 15638–15643. doi: 10.1073/pnas.242590799 CrossRef Google Scholar Laurent VM, Henon S, Planus E, Fodil R, Balland M, Isabey D, Gallet F (2002) Assessment of mechanical properties of adherent living cells by bead micromanipulation: comparison of magnetic twisting cytometry vs optical tweezers. J Biomech Eng 124(4): 408–421.

doi: 10.1115/1.1485285 CrossRef Google Scholar Maepea O, Bill A (1992) Pressures in the juxtacanalicular tissue and Schlemm’s canal in monkeys. Exp Eye Res 54(6): 879–883. doi: 10.1016/0014-4835(92)90151-H CrossRef Google Scholar Mathur AB, Collinsworth AM, Reichert WM, Kraus WE, Truskey GA (2001) Endothelial, cardiac muscle and skeletal muscle exhibit different viscous and elastic properties as determined by atomic force microscopy. J Biomech 34(12): 1545–1553. doi: 10.1016/S0021-9290(01)00149-X CrossRef Google Scholar Mathur AB, Reichert WM, Truskey GA (2007) Flow and high affinity binding affect the elastic modulus of the nucleus, cell body and the stress fibers of endothelial cells.

Ann Biomed Eng 35(7): 1120–1130. doi: 10.1007/s10439-007-9288-8 CrossRef Google Scholar Matthews BD, Overby DR, Alenghat FJ, Karavitis J, Numaguchi Y, Allen PG, Ingber DE (2004) Mechanical properties of individual focal adhesions probed with a magnetic microneedle. Biochem Biophys Res Commun 313(3): 758–764. doi: 10.1016/j.bbrc.2003.12.005 CrossRef Google Scholar Mijailovich SM, Kojic M, Zivkovic M, Fabry B, Fredberg JJ (2002) a finite element model of cell deformation during magnetic bead twisting. J Appl Physiol 93(4): 1429–1436 Google Scholar Miyazaki H, Hayashi K (1999) Atomic force microscopic measurement of the mechanical properties of intact endothelial cells in fresh arteries.

Med Biol Eng Comput 37(4): 530–536. doi: 10.1007/BF02513342 CrossRef Google Scholar Oden JT (1967) Mechanics of elastic structures. McGraw-Hill, New York Google Scholar Ohayon J, Tracqui P (2005) Computation of adherent cell elasticity for critical cell-bead geometry in magnetic twisting experiments. Ann Biomed Eng 33(2): 131–141. doi: 10.1007/s10439-005-8972-9 CrossRef Google Scholar Ohayon J, Tracqui P, Fodil R, Fereol S, Laurent VM, Planus E, Isabey D (2004) Analysis of nonlinear responses of adherent epithelial cells probed by magnetic bead twisting: A finite element model based on a homogenization approach. J Biomech Eng 126(6): 685–698.

doi: 10.1115/1.1824136 CrossRef Google Scholar Overby DR, Matthews BD, Alsberg E, Ingber DE (2005) Novel dynamic rheological behavior of individual focal adhesions measured within single cells using electromagnetic pulling cytometry. Acta Biomater 1(3): 295–303. doi: 10.1016/j.actbio.2005.02.003 CrossRef Google Scholar Quigley HA, Broman AT (2006) The number of people with glaucoma worldwide in 2010 and 2020. Br J Ophthalmol 90(3):262–267. see comment. doi: 10.1136/bjo.2005.081224 Read AT, Chan DW, Ethier CR (2007) Actin structure in the outflow tract of normal and glaucomatous eyes. Exp Eye Res 84(1): 214–226.

doi: 10.1016/j.exer.2005.10.035 CrossRef Google Scholar Sato H, Kataoka N, Kajiya F, Katano M, Takigawa T, Masuda T (2004) Kinetic study on the elastic change of vascular endothelial cells on collagen matrices by atomic force microscopy. Colloids Surf B Biointerfaces 34(2): 141–146. doi: 10.1016/j.colsurfb.2003.12.013 CrossRef Google Scholar Sato M, Nagayama K, Kataoka N, Sasaki M, Hane K (2000) Local mechanical properties measured by atomic force microscopy for cultured bovine endothelial cells exposed to shear stress. J Biomech 33(1): 127–135.

doi: 10.1016/S0021-9290(99)00178-5 CrossRef Google Scholar Sato M, Theret DP, Wheeler LT, Ohshima N, Nerem RM (1990) Application of the micropipette technique to the measurement of cultured porcine aortic endothelial cell viscoelastic properties. J Biomech Eng 112(3): 263–268. doi: 10.1115/1.2891183 CrossRef Google Scholar Schrot S, Weidenfeller C, Schaffer TE, Robenek H, Galla HJ (2005) Influence of hydrocortisone on the mechanical properties of the cerebral endothelium in vitro. Biophys J 89(6): 3904–3910.

doi: 10.1529/biophysj.104.058750 CrossRef Google Scholar Solon J, Levental I, Sengupta K, Georges PC, Janmey PA (2007) Fibroblast adaptation and stiffness matching to soft elastic substrates. Biophys J 93(12): 4453–4461. doi: 10.1529/biophysj.106.101386 CrossRef Google Scholar Stamer WD, Roberts BC, Howell DN, Epstein DL (1998) Isolation, culture, and characterization of endothelial cells from Schlemm’s canal. Invest Ophthalmol Vis Sci 39(10): 1804–1812 Google Scholar Theret DP, Levesque MJ, Sato M, Nerem RM, Wheeler LT (1988) The application of a homogeneous half-space model in the analysis of endothelial cell micropipette measurements.

J Biomech Eng 110(3): 190–199 CrossRef Google Scholar Underwood JL, Murphy CG, Chen J, Franse-Carman L, Wood I, Epstein DL, Alvarado JA (1999) Glucocorticoids regulate transendothelial fluid flow resistance and formation of intercellular junctions. Am J Physiol 277(2 Pt 1): C330–C342 Google Scholar Wang N, Butler JP, Ingber DE (1993) Mechanotransduction across the cell surface and through the cytoskeleton. Science 260(5111): 1124–1127. doi: 10.1126/science.7684161 CrossRef Google Scholar Wang N, Ingber DE (1995) Probing transmembrane mechanical coupling and cytomechanics using magnetic twisting cytometry. Biochem Cell Biol 73(7–8): 327–335 CrossRef Google Scholar Yih C (1988) Fluid Mechanics: a concise introduction to the theory.

West River Press, Ann Arbor Google Scholar Zeng D, Juzkiw T, Ethier CR, Johnson M (2007) Estimating Young’s modulus of Schlemm’s canal endothelial cells. ARVO, Ft. Lauderdale Google Scholar Copyright information

Question: Where in the body would you find the 'Canal of Schlemm'?
Answer: IN THE EYE