|
|
| Glaucoma is generally associated with high pressure in the eyes, but many cases of glaucoma occur in the absence of high pressure readings during exams. |
|
|
FREQUENCY
Normal tension glaucoma is a fairly common problem. There have been a number of different studies trying to determine its frequency, but it appears that around one-third of all glaucoma patients have low-tension glaucoma. Some studies have even shown that more than 50-percent of glaucoma cases may be low tension.
|
|
RISK FACTORS
Various factors increase the risk of developing low-tension glaucoma. Age, a family history of open angle or low-tension glaucoma are considered risk factors. Of course, intra-ocular pressure is considered a risk factor, and the higher the pressure, the greater the risk. Optic nerve hemorrhages, atrophy around the optic nerve itself and nearsightedness are thought to be additional risk factors for developing low-tension glaucoma.
|
Twenty percent of those with low-tension glaucoma have optic nerve hemhorrhages, compared with just four percent of those with open angle glaucoma, and less than one percent of patients with no glaucoma.
Systemic factors include migraine headaches and a tendency toward cold hands and feet. Both are thought to reflect a tendency toward vascular spasm, which can be a contributing factor in low-tension glaucoma.
|
|
CAUSE
Intra-ocular pressure is thought to be a factor. The mechanical theory of glaucoma and optic nerve damage is that increased intra-ocular pressure distorts the supporting tissue of the optic nerve and causes compression damage to the nerve fibers and interference with the nerve fibers.
In this theory it is thought that normal tension glaucoma patients may have a weakness in the structural elements of the nerve itself. Relatively normal pressures are then able to cause damage.
|
| Another theory involves relative lack of blood supply to the optic nerve that eventually destroys the nerve fibers. The precise role of vascular factors in normal tension glaucoma is not entirely clear, but many believe it represents at least a partial explanation of the problem in some patients. |
Another consideration is that nerve fiber layers simply atrophy and die over the years in some patients, similar to the way that the tissue beneath the surface of the skin tends to disappear over the years with sagging of the tissue.
It may then be associated with aging and a process which is more than accelerated in some patients than in others.
It is quite probable that a combination of factors mechanical, vascular, and possibly spontaneous nerve fiber atrophy are involved.
|
|
DIFFERENTIAL DIAGNOSIS
There are a number of things that masquerade as low-tension glaucoma, including intermittent pressure elevation. In other words, some patients at times may have a pressure elevation that caused the problem, but under office testing conditions, it simply has not been identified.
This could be the result of just brief intermittent elevations, or long-term fluctuations in pressure elevations that have been masked by systemic medications such as beta-blockers.
|
The condition of low-tension glaucoma can also result from previous elevations of pressures that are now gone but have left the optic nerve looking abnormal. Examples include a period of topical steroid use in the eyes, inflammation of the eyes, trauma or prior elevated pressure with “burned out” glaucoma.
Other possible factors are conditions that compress the optic nerve, birth abnormalities that masquerade as glaucomatous optic nerve damage and nutritional abnormalities.
|
| Systemic vascular disease can also cause optic nerve damage and visual field loss including ischemic optic neuropathy and carotid artery disease, which may limit adequate blood flow to the optic nerve.
Ischemic optic neuropathy represents a sudden shutdown of the blood supply to the nerve, leaving it pale and cupped.
An additional cause can be hemodynamic crisis; for example, severe blood loss associated with a prior surgery, or an accident which may have caused a stroke-like syndrome within the optic nerve.
|
|
TREATMENT
While intra-ocular pressure may not be the only factor in low-tension glaucoma, we believe it does participate in the production of damage. Therefore, lowering the pressure should be the logical therapeutic goal, since it represents the only form of treatment we have available at this time.
The typical approach is to identify a target pressure, then use medical therapy, laser treatment or even surgery if necessary, to achieve that pressure.
|
| Quality of life issues are important in choosing a treatment plan. If medications are creating a major problem with the quality of life, or low pressure is not achieved, then laser treatment is considered. If laser does not work satisfactorily, we consider glaucoma surgery. |
We recognize that surgery generally carries a greater risk than medical treatment. We may accept a compromise and not achieve quite the degree of pressure-lowering we want, rather than proceeding to filtering surgery.
If pressures are clearly not being controlled adequately, or we are dealing with progressive loss, then filtering surgery remains a consideration.
There is some disagreement about the benefit of filtering surgery, but again, lowering the pressure is typically the only treatment alternative that is available.
|
|