The loss of ganglionic cells and their axons is also defined as glaucomatous damage. When an atrophy of the papilla occurs, glial cells and blood vessels are irreversibly damaged, as well as the nerve fibres of the optic disk. This leads to the excavation, a depression in the centre of the optic disk. The functional damage which follows is characterized by defects in the visual field difficult to perceive by the patient, at least in the early stages of the disease.
Various factors contribute to the glaucomatous damage; the most important ones being an increase of ocular pressure and a reduction of the ocular hematic flow.
Many and various causes explain the increase of intraocular pressure (IOP). In congenital glaucoma, the angle of the anterior chamber is not completely developed. When the angle has mostly developed, but is still abnormal, IOP rises in infancy (infantile glaucoma) or in the teenage years (juvenile glaucoma). In primary open-angle glaucoma (POAG), the IOP is high even if the angle of the anterior chamber is developed and opened, and without concomitant pathologies. The rise of IOP is due to the increase of resistence to the reflux. POAG is by far the most common form of glaucoma and is particularly frequent among seniors. Rise of IOP slowly proceeds without the patient noticing it. Particularly in the early stages of the disease, the patient does not realize the defects in the visual field. In closed-angle glaucoma, there is a sudden and unexpected rise of IOP due to a rapid and complete obstruction of the chamber's angle by the iris. Symptoms are more severe. IOP can still rise because of a pseudoexfoliation syndrome or because of a pigment dispersion syndrome.
A secondary increase of IOP can be due
to certain medication, inflammation and complications from diabetic
retinopathy, occlusive retinal vasculitis, and other ocular diseases.A condition which increases the probability of a certain event is defined as a factor of risk. We have to distinguish the factors of risk which create an increase of IOP from the factors of risk which can damage the optic nerve.
The primary factors of risk for IOP are: age, family history, race and artheriosclerosis. Primary factors of risk for glaucomatous damage are: rise in IOP, vascular disturbance with systemic low blood pressure and vasospasm, myopia and race.
In glaucoma, nerve cells and ganglionic cells die principally because of a process called apoptosis or programmed cell death. Apoptosis is probably initiated by a reduced flow of axon-released information and by circulatory problems. These perfusion problems may be caused by a high IOP or by low blood pressure, particularly when a flawed autoregulation is incapable of maintaining perfusions at constant levels. The reperfusion phase following the reduced perfusion is probably more damaging than the ischemia itself. This explains the particular damaging effect of the fluctuations of IOP and blood pressure. The damage from reperfusion depends on the formation of free radicals, which also cause a rise in glutamate at toxic levels.
To diagnose glaucomatous damage, particularly in the early phases of the disease, can be considered a challenge. The diagnosis is based above all on the analysis of the optic disk and on the visual field test. The systematic measurement of the visual field function, called perimetry, is the most important method of evaluating the progression of glaucomatous damage. The eye specialist also has to study the factors of risk measuring, for exemple, intraocular pressure while controlling the interior chamber's angle to avoid its closure. Circulation will be attentively evaluated and possibly quantified if it is suspected that a problem of perfusion has a role in the pathogenesis of the damage.
Appropriate methods to do this are the blood pressure measurement, the eco-colour-doppler, and capillaroscopy. Even if other exams are useful to provide information on alterations caused by glaucoma, they are not done routinely because they do not contribute in a determinant way to the diagnosis and to the evaluation of the progression of glaucomatous damage. Ulterior loss of visual function can manisfest itself in the difficulty to adapt to light, in alterations of the chromatic sense and sensitivity to contrasts, and a strong sensation of dazzle. There may also be changes in the electrophysiological exams: ERG and VECP.
Many patients with glaucoma do not complain of any symptoms at the moment of diagnosis. However, they are treated with medication which can potentially present side effects. These unfavourable reactions may be possible with medication therapy as well as with surgery. The patient with glaucoma may have to accept a loss in quality of life in order to ensure a stable visual function in the future.
The spectrum of therapeutic possibilities has widened enormously in the last years.
There is a lot of medication helping to reduce IOP, and each one of those represents advantages and disadvantages. Therapy for each patient is chosen within this wide spectrum of choices taking into account individual requirements and situation.
Laser treatment appears to be of minor importance in glaucoma therapy. Laser iridotomy is used essentially in preventing an attack of closed-angle glaucoma. Surgery is necessary in those cases where glaucoma progresses even after medical therapy. There are various technical surgeries, and also for these there are advantages and disadvantages. Post-surgery treatment for the patient is as important as the surgery itself.
For some patients, it is not sufficient to lower the intraocular pressure; it is necessary to have a better ocular perfusion. This means, first of all, that sudden fall of blood pressure has to be avoided. The medical treatment for blood pressure is inevitable when it cannot be lowered with regular cures. There exist many drugs to reduce vascular disturbance and their efficiency and tolerance depends on the individual situation of the patient. There is also alternative therapy but experience has so far demonstrated that it is quite limited in treating glaucoma.