[Contemporary possibilities and perspectives in the treatment of glaucoma]

The aim of this paper is to present and discuss the contemporary possibilities and perspectives of applying neuroprotective mechanisms in the treatment of glaucoma.

A review of the newest concepts concerning neuroprotective action of antiglaucoma drugs was done.

Not until recently was it believed that glaucoma is caused by an increased intraocular pressure. When it comes to diagnosing glaucoma it is nowadays considered that intraocular pressure is not the most important factor. Glaucoma is presently regarded as a condition in which characteristic changes in the appearance of the optic disc and distinctive progressive changes in the visual field occur because of progressive and irreversible destruction of the retinal ganglion cells. Intraocular pressure may sometimes, but not necessarily, accompany those changes. Hence, it is thought that neuroprotection in glaucoma is aimed at delaying or blocking the mechanisms of ganglion cell degeneration. Two groups of antiglaucoma drugs with neuroprotective action can be distinguished, depending on whether neroprotective action is direct or indirect. Drugs with direct neuroprotective action are more effective at preventing changes created by glaucoma. However, the majority of antiglaucoma drugs act indirectly. Sympatholytics, carbonic anhydrase inhibitors, analogs of prostaglandins, parasympathicomimetics, sympathicomimetics as well as hyperosmotic agents lower intraocular pressure and lead to an increase in blood flow through vessels of the retina and optic nerve. Therefore, almost all antiglaucoma drugs in an indirect way delay the process of gradual and irreversible degeneration of retinal ganglion cells. Only a few antiglaucoma drugs show direct neuroprotective action, among them betaxolol, metipranolol, brimonidine and clonidine. Additionally, calcium-channel blockers are generally administered in the treatment of glaucoma. One may anticipate that newer and more effective antiglaucoma drugs will be available in future. Possibly, mechanisms of direct neuroprotection will be exploited in their design. Glaucoma treatment may be based on NMDA, AMPA, kainate or metabotropic antagonists. Moreover, nitric oxide inhibitors, growth factors, neurotrophins, gangliosides or antioxidants emerge as candidate antiglaucoma drugs.