What is Glaucoma?
Chat Highlights
April 4, 2007

On Wednesday, April 4, 2007, Dr. Rick Wilson, a glaucoma specialist at Wills, and the glaucoma chat group discussed "What is Glaucoma?"

Moderator:  Welcome back, Dr. Wilson.  How is glaucoma defined?

Dr. Rick Wilson:  Glaucoma is a group of diseases that causes characteristic optic nerve damage and visual field changes.  IOP (intraocular pressure) is one of the primary risk factors.

P:    How does the type of glaucoma affect the rate of the glaucoma progression?  Which types progress faster?

Dr. Rick Wilson:  Clearly, glaucomas, such as acute-angle closure, which characteristically has high IOP, will progress faster.  The secondary glaucomas, such as traumatic, inflammatory, or secondary to steroids, often evidence high IOPs.  When they occur in a patient with low resistance to damage from IOP, the damage may progress rapidly.

P:  You say that glaucoma is a group of diseases.  Are the types clearly distinguishable?

Dr. Rick Wilson:  No.  Glaucoma seems to be a spectrum of disease, with variable factors causing the damage.  We are starting to recognize differences in the way the optic nerve and visual field are damaged and have a greater appreciation for the range of harmful factors.

P:  What is the characteristic change to the optic nerve?

Dr. Rick Wilson:  If the IOP is quite high, say 50’s or above, for a period of several weeks, the nerve becomes pale, possibly more so in some areas than in others.  The cupping, or depression, in the center of the optic nerve, which we think is characteristic of glaucoma, is absent.  Usually, though, a lower IOP than is seen with acute angle-closure glaucoma, but is still abnormally high, will, over the years, result in a gradual thinning of the nerve fiber layer overlying the retina and a loss of optic nerve.

P:  What, besides high IOP, damages the optic nerve and visual field?

Dr. Rick Wilson:  High IOP is the usual factor, but blood circulation factors, such as low systemic blood pressure or spasm of the vessel carrying blood to the optic nerve, can damage the nerve in the face of normal IOP.  Some areas of the retina are more easily damaged than others.  The retina dies in a characteristic pattern.  As areas of the retina cease to work, that part of the visual field is no longer seen and characteristic glaucomatous visual field loss ensues.

P:  How do you try to raise the systemic blood pressure?

Dr. Rick Wilson:  Salt tablets, V-8 juice before bedtime, and mineral corticoid drugs are usually tried.

P:  What happens to the cells in the retina and the optic nerve?

Dr. Rick Wilson:  Simply put, the rods and cones in the retina, which process the light entering the eye, pass that information to overlying retinal ganglion cells.  The body of the cell is in the retina, but the long tail of the cell is the fiber that carries the light-impulse information back to the first part of the brain.  As the retinal ganglion cells are slowly injured and die, both the body and the tail, or nerve fiber (which runs back to the brain and make up the optic nerve), atrophy or lose form and disappear.  The retinal nerve-fiber layer thins, giving the optic nerve the characteristic cup.

P:  Once the retina and optic nerve cells die, can they be revived?

Dr. Rick Wilson:  Those are neural cells and, like the brain, once mortally injured, cannot be revived.  However, there seems to be a state when the retinal ganglion cell is injured to the point that it is not functioning, but is not yet dead. If the IOP is lowered dramatically, or the circulation increased, cells in that state may start to function again.  The visual fields may actually improve slightly.

P:  Can you tell from the pattern of visual field loss what type of glaucoma the patient has and how quickly the loss will continue?

Dr. Rick Wilson:  There are only a few kinds of glaucoma, such as normal-tension glaucoma, where the visual field may be characteristic enough to give a diagnosis.  If the eye doctor has a history of the patient’s IOPs and all the corresponding visual field tests, he or she should be able to offer an opinion about how fast the visual field will worsen at an IOP in the range at which the patient has previously demonstrated loss.

P:  What is the characteristic visual field loss and progression for normal-tension glaucoma?

Dr. Rick Wilson:  Patients with normal-tension glaucoma often have visual field defects that are unusually close to the center of the visual field.  Often these defects get progressive denser.  The patient can only see brighter and brighter lights in that area, but the defect may not get much bigger.

P:  In POAG (primary open-angle glaucoma), is the progression of damage fairly linear and constant, or is it more stop and go, with long periods of no change?

Dr. Rick Wilson:  The progression is variable.  It seems to be related to the height of the IOP in most, but not all, people.  In the early stages, loss is usually slowly linear if the IOP is too high for the optic nerve to withstand and constant. In later stages, progression may speed up.  When the nerve is severely damaged, progression may become more step-like.

P:  I'm a complete novice, but would like to understand the basics of interpreting my visual field tests.  Can you suggest any reading material?

Dr. Rick Wilson:  As I remember, Dr. Jeff Henderer has had a couple chats about the visual field.  The highlights of those chats are good resources.  [Editor’s note: Also see “Understanding Visual Field Testing” by Jeffrey Henderer, M.D. http://www.willsglaucoma.org/testing/vf.html ]  

P:  Since glaucoma is influenced or caused by so many different factors, why is that historically the treatment approach has been to lower intraocular pressure?  I know that more recently, research has begun to investigate genetic factors.  What fundamentally different results do you think that approach could bring?

Dr. Rick Wilson:  Unfortunately, the IOP is the main risk factor we can control, and it seems to play a role in almost all patients.  For years, we have tried to control vessel spasms, which seem to play a role in some people, with only minimal success.  We also try to raise the systemic blood pressure in patients who have too low a blood pressure at night.  We use our present state of genetic knowledge to help us diagnose patients and maybe tell how aggressive their disease is. In the future, genetic therapy will probably play as big a role or bigger than stem cells.

P:  I may be one of those patients whose eye damage was the outcome of arterial spasm.  Yet treatment options for me (pressure-lowering medications or surgery) seem indifferent to the cause of my problem.  I'm greatly troubled by this state of affairs in ophthalmology, especially since treatments I've tried so far have been, not only ineffective, but also adverse experiences. Is there anyone out there really thinking about my kind of glaucoma?

Dr. Rick Wilson:  Yes, I think a great number of people are.  In all but a handful of patients I have had, lowering the IOP low enough for them stopped their progression.  However, as you mention, lowering IOP often to lower than normal levels results in a multitude of side effects, some worse than others (e.g., cataracts).  Many people are trying to understand the causative factors for glaucoma better and how they work together.  There is some evidence that glaucoma is a systemic disease, so a whole body view is a necessity.

Moderator:  When glaucoma may be caused by arterial spasm, why would the glaucoma continue to worsen once the event is over?

Dr. Rick Wilson:  The spasm is usually recurrent.

P:  Is arteritis the same as arterial spasm?

Dr. Rick Wilson:  No.  Examples of arterial spasm are Raynaud's syndrome or migraines. Arteritis is usually an inflammation of the artery wall that narrows or blocks the lumen of the vessel, for example, giant cell arteritis.

P:  Many glaucoma patients in the U.S. have had their IOPs measured at intervals during the daytime only.  Since higher IOPs at night might compromise optic nerve circulation, how much does it help the doctor to know what the diurnal curve is during daylight hours?

Dr. Rick Wilson:  We have recently discovered that IOPs are routinely higher during the night, often just at awakening in the morning.  Lying supine (on the back) elevates the venous blood pressure around the eye and elevates the IOP.  Knowing the daytime IOP curve can help if the IOP is variable.  That is, a curve over 5 mm would be suspicious in a glaucoma suspect, or a rise above target IOP, would explain a worsening with normal IOPs in the usual office checks.

P:  Is there any connection between narrow-angle glaucoma and Viagra-type drugs?

Dr. Rick Wilson:  Not that I know of.  The changes in vision that have been seen with Viagra are related to optic nerve circulation.

P:  Is progression of glaucomatous neuropathy always prevented or slowed by reducing IOP?

Dr. Rick Wilson:  Rarely, it is not.  However, the usual mistake is not to lower the IOP enough to make a difference.

P:  Since a relationship between normal-tension glaucoma and migraine has been observed to some extent, has there been any research on treatment of normal-tension glaucoma with medications for migraine?

Dr. Rick Wilson:  Yes, but calcium channel blockers have been employed most often.

Moderator:  Thank you, Dr. Wilson, for sharing your knowledge with us tonight.

On April 18, Dr. Pro discussed "Risk Factors for Glaucoma" in the Chat room. Click here for highlights of that meeting.

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