Preface

Glaucoma is a family of diseases that includes primary open angle glaucoma (POAG), normal tension glaucoma (NTG), angle-closure glaucoma, secondary glaucoma and glaucoma with onset in infancy. The effect of glaucoma is the death of retinal ganglion cells (RGCs) which causes ultimate loss of vision. The nature of glaucomatous visual field changes and morphologic abnormalities suggests that the pathophysiology reflects injury which occurs at the level of the optic nerve. It remains a matter of debate as to whether this is caused by ischemia at the optic nerve head, blockade of ganglion cell axonal transport, peripapillary atrophy, or changes in the characteristics of the lamina cribosa. Loss of RGCs in glaucoma, especially in POAG and NTG, is gradual with some cells dying ten to twenty years later than others. The challenge for the future is therefore to devise ways of preventing functional RGCs dying once glaucoma is diagnosed.

Glaucoma has traditionally been diagnosed by either elevated intraocular pressure (IOP), optic nerve head atrophy of a defined clinical characteristic, or ‘‘cupping’’ and loss of visual field. The current treatment strategy involves medical, surgical, or parasurgical interventions, all aimed at reducing the IOP. This is now widely acknowledged to be insufficient, as many glaucoma patients progress despite treatment and many patients do not have elevated IOP in the first place.

Over the past three decades much research has been devoted to discovering novel therapeutic strategies to improve the clinical outcome of the vast majority of patients with glaucoma. In particular, numerous studies have aimed at identifying pharmacological agents that can directly attenuate RGC death as occurs in glaucoma. Much has been learned from experimental studies on animal models of glaucoma and from information related to the treatment of other CNS degenerative diseases.

Unfortunately, a large clinical trial stimulated by impressive experimental studies has proved unsuccessful, raising many questions related to neuroprotection strategies for the treatment of glaucoma. It is clear that further progress is necessary before it is possible to translate basic science into clinically effective technologies. Moreover, this goal can only be reached through the development of suitable procedures to monitor disease onset and progression.

In this book, leaders in the field of glaucoma contribute articles which shed light on current ideas about the pathophysiology of the disease where putative risk factors require serious consideration. Suitable sensitive procedures for diagnosis and clinical monitoring of the disease need particular thought in order to demonstrate whether a neuroprotection strategy is possible. Topics include experimental models of glaucoma, clinical protocols for the study of neuroprotective therapies, mechanisms underlying glaucomatous damage to neurons of the retina and other ‘‘relay stations’’ in the visual pathway in the brain, and, last but not least, future insights into ways of preventing neuronal injury in glaucoma patients.

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