Обоснование нейропротекции при глаукоме

Abstract

Glaucoma is a chronic progressive optic neuropathy, characterized by changes in the optic nerve head (cup) and ganglion cell complex (GCC) loss that lead to field of vision defects. In some patients GCC loss progresses despite intraocular pressure (IOP) level normalization. Today neuroprotection is one of the most promising trends in glaucoma treatment. It is directed at GCC loss prevention in patients with normal-tension glaucoma. Neuroprotection can be direct or indirect, depending on the nature of damaging factors and counteraction mechanisms. Indirect neuroprotection includes IOP level decrease and hemodynamics improvement. Direct neuroprotection can be primary and secondary. Such pharmaceutical groups as NMDA-receptor antagonists and calcium-channel blockers have a direct neuroprotective action. They protect retinal neurons and optic nerve head fibers by blocking the main ischemic cell damage factors and moderate ischemia-associated increase of lipid peroxidation products, free radicals and calcium ions concentration. Secondary neuroprotection drugs influence the delayed neuronal death mechanisms. They include Ginkgo biloba, antioxidants, neurotrophic drugs (Brimonodone, Betaxolol, carbonic anhydrase inhibitors, prostaglandin analogues) and peptide bioregulators. IOP level decrease still remains the main means of glaucoma treatment. One of the questions of considerable substance in IOP lowering achievement is the elaboration of alternative methods aimed at further progression prevention. Based on the latest research, neuroprotective medicine shows promise in GCC loss prevention despite the actual IOP level. This article presents information on a wide range of neuroprotective drugs used in complex glaucoma treatment.