Glaucoma Support Group

Glaucoma is a group of diseases of the optic nerve involving loss of retinal ganglion cells in a characteristic pattern of optic neuropathy. Although raised intraocular pressure is a significant risk factor for developing glaucoma, there is no set threshold for intraocular pressure that causes glaucoma. One person may develop nerve damage at a relatively low pressure, while another person may have high eye pressures for years and yet never develop damage. Untreated glaucoma leads to permanent damage of the optic nerve and resultant visual field loss, which can progress to blindness.

While glaucoma may or may not have distinct symptoms, an almost inevitable complication of glaucoma is vision loss. Visual loss from glaucoma first affects peripheral vision. Early vision loss is subtle, and is not noticed by the patient. Moderate to severe vision loss may be noticed by the patient by checking his peripheral vision thoroughly. This can be done by closing one eye and examining all four corners of the visual field for clarity and sharpness, then repeating with the other eye closed. All too often, the patient does not notice the loss of vision until he experiences "tunnel vision". If the disease is not treated, the visual field will become more and more narrow, obscuring central vision, and finally progressing to blindness in the affected eye(s).

Waiting for symptoms of visual loss to occur is not optimal care. Visual loss related to glaucoma is irreversible, but can be prevented or slowed by treatment. An optometrist or ophthalmologist should be consulted by people at risk for glaucoma.

Although intraocular pressure is only one of the causes of glaucoma, lowering it via pharmaceuticals or surgery is currently the mainstay of glaucoma treatment. In Europe, Japan, and Canada laser treatment is often the first line of therapy. In the U.S., adoption of early laser has lagged, even though prospective, multi-centered, peer-reviewed studies, since the early '90's, have shown laser to be at least as effective as topical medications in controlling intraocular pressure and preserving visual field.

Intraocular pressure can be lowered with medication, usually eye drops. There are several different classes of medications to treat glaucoma with several different medications in each class. Topical beta-adrenergic receptor antagonists such as timolol, levobunolol (Betagan) , and betaxolol decrease aqueous humor production by the ciliary body. Alpha2-adrenergic agonists such as brimonidine (Alphagan) work by a dual mechanism, decreasing aqueous production and increasing uveo-scleral outflow. Less-selective sympathomimetics like epinephrine and dipivefin (Propine) increase outflow of aqueous humor through trabecular meshwork and possibly through uveoscleral outflow pathway, probably by a beta2-agonist action. Miotic agents (parasympathomimetics) like pilocarpine work by contraction of the ciliary muscle, tightening the trabecular meshwork and allowing increased outflow of aqueous through traditional pathways. Carbonic anhydrase inhibitors like dorzolamide (Trusopt), brinzolamide (Azopt), acetazolamide (Diamox) lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body. Prostaglandin analogs like latanoprost (Xalatan), bimatoprost (Lumigan) and travoprost (Travatan) increase uveoscleral outflow of aqueous. Each of these medicines may have local and systemic side effects. Adherence to the medication protocol can be confusing and expensive; if side effects occur, the patient must be willing either to tolerate these, or to communicate with the treating physician to improve the drug regimen.

Poor compliance with medications and follow-up visits is a major reason for vision loss in glaucoma patients. Patient education and communication must be ongoing to sustain successful treatment plans for this lifelong disease with no early symptoms.

Marijuana has been shown to lower the intraocular pressure in some eyes in a few studies but this is generally not used clinically. Studies in the early 1970s showed that marijuana, when smoked, lowers intraocular pressure in people with normal pressure and those with glaucoma. In an effort to determine whether marijuana, or drugs derived from marijuana, might be effective as a glaucoma treatment, the National Eye Institute supported research studies from 1978 to 1984. These studies demonstrated that some derivatives of marijuana lowered intraocular pressure when administered orally, intravenously, or by smoking, but not when topically applied to the eye. However, none of these studies demonstrated that marijuana -- or any of its components -- could safely and effectively lower intraocular pressure any more than a variety of drugs then on the market.

The possible neuroprotective effects of various topical and systemic medications are also being investigated.