Glaucoma is a spectrum of clinical entities that encompassesmany ocular and systemic conditions. It may be a primary eye disease, or a manifestation of some other ocular or systemic disease.
The change in the definition of glaucoma from a pressure disease to an optic neuropathy, intraocular pressure as a risk factor rather than the cause of glaucoma, new methods for early detection and diagnosis of glaucoma (‘pre-perimetric’), and a solid scientific basis for approaches to treatment (based upon a number of landmark clinical studies).
Around the time of the publication of the First Edition, ophthalmologists had begun to recognize that glaucoma is an optic nerve disease, with ‘characteristic’ progressive structural changes leading to loss of visual function in a ‘characteristic’ way. The use of intra - ocular pressure levels to define the disease has pretty much gone away, and now pressure is used to gauge the risk of having, or developing, glaucoma. Does that mean that the 65-year-old patient with ‘cupped out’ optic nerves, central and temporal islands in the visual fields, and an untreated intraocular pressure of 12 mmHg has glaucoma, while the 45-year-old myopic male with pigment dispersion syndrome and an initial intraocular pressure of 52 mmHg in each eye with normal optic nerves and visual fields doesn’t? The former patient may be in the ‘burned out’ stage of glaucoma or may have suffered visual loss from anterior ischemic optic neuropathy, while the latter may be in the early stages of glaucoma or may have simply had a transient rise in pressure following a brisk walk. To try to describe multiple disease, conditions, and scenarios in a widely disparate group of patients with a single term ‘glaucoma’ is subject to frustration.
Comprehension of glaucoma’s pathophysiology is improving, but there is much we don’t know. We are well into a new era in glaucoma research, focusing on the cellular mechanisms responsible for the death of optic nerve axons. The research is proceeding on many different fronts: genetic, biochemical, and cellular biological, to name but a few. New ideas are emerging. Perhaps intraocular pressure (in some people) is the initiating event that damages a handful of neurons, with the bulk of the damage then done by the propagation of environmental toxins released when those cells die. Perhaps glaucoma is the genetically predetermined self-destruction of the optic nerve, with similar genetically determined mechanisms in the trabecular meshwork responsible for the observed increase in intraocular pressure, with no causal relationship between intraocular pressure and optic nerve damage. Perhaps glaucoma is a condition in which the blood flow to the optic nerve is insufficient for its nutritional requirements, leading to its ultimate demise. How different these ideas are from the concept that ‘glaucoma is a disease in which the intraocular pressure rises and this causes optic nerve damage’.
This book illustrates about ‘glaucoma’ today. It encompasses a wide variety of subjects, as one would expect for a disease that encompasses a wide variety of clinical conditions, syndromes, and findings.
The change in the definition of glaucoma from a pressure disease to an optic neuropathy, intraocular pressure as a risk factor rather than the cause of glaucoma, new methods for early detection and diagnosis of glaucoma (‘pre-perimetric’), and a solid scientific basis for approaches to treatment (based upon a number of landmark clinical studies).
Around the time of the publication of the First Edition, ophthalmologists had begun to recognize that glaucoma is an optic nerve disease, with ‘characteristic’ progressive structural changes leading to loss of visual function in a ‘characteristic’ way. The use of intra - ocular pressure levels to define the disease has pretty much gone away, and now pressure is used to gauge the risk of having, or developing, glaucoma. Does that mean that the 65-year-old patient with ‘cupped out’ optic nerves, central and temporal islands in the visual fields, and an untreated intraocular pressure of 12 mmHg has glaucoma, while the 45-year-old myopic male with pigment dispersion syndrome and an initial intraocular pressure of 52 mmHg in each eye with normal optic nerves and visual fields doesn’t? The former patient may be in the ‘burned out’ stage of glaucoma or may have suffered visual loss from anterior ischemic optic neuropathy, while the latter may be in the early stages of glaucoma or may have simply had a transient rise in pressure following a brisk walk. To try to describe multiple disease, conditions, and scenarios in a widely disparate group of patients with a single term ‘glaucoma’ is subject to frustration.
Comprehension of glaucoma’s pathophysiology is improving, but there is much we don’t know. We are well into a new era in glaucoma research, focusing on the cellular mechanisms responsible for the death of optic nerve axons. The research is proceeding on many different fronts: genetic, biochemical, and cellular biological, to name but a few. New ideas are emerging. Perhaps intraocular pressure (in some people) is the initiating event that damages a handful of neurons, with the bulk of the damage then done by the propagation of environmental toxins released when those cells die. Perhaps glaucoma is the genetically predetermined self-destruction of the optic nerve, with similar genetically determined mechanisms in the trabecular meshwork responsible for the observed increase in intraocular pressure, with no causal relationship between intraocular pressure and optic nerve damage. Perhaps glaucoma is a condition in which the blood flow to the optic nerve is insufficient for its nutritional requirements, leading to its ultimate demise. How different these ideas are from the concept that ‘glaucoma is a disease in which the intraocular pressure rises and this causes optic nerve damage’.This book illustrates about ‘glaucoma’ today. It encompasses a wide variety of subjects, as one would expect for a disease that encompasses a wide variety of clinical conditions, syndromes, and findings.
Contents
1 Introduction to glaucoma
2 Classification of glaucoma
3 Aqueous humor dynamics
4 Intraocular pressure and its measurement
5 Gonioscopy
6 The optic nerve in glaucoma
7 Scanning laser imaging
8 Psychophysical and electrophysiological testing in glaucoma: visual fields and other functional tests
9 Primary open-angle glaucoma
10 Secondary open-angle glaucomas
11 The angle-closure glaucomas
12 Normal-tension glaucoma
13 Ocular blood flow
14 The developmental glaucomas
15 Medical therapy for glaucoma
16 Laser surgery in the treatment of glaucoma
17 Filtering surgery
18 Non-penetrating surgery
19 Aqueous shunts
20 Combined cataract and glaucoma surgery
21 Treatment of developmental glaucoma
Index
Book Details
- Author: T. Choplin Neil and Diane C. Lundy
- Hardcover: 159 pages
- Publisher: Informa Healthcare; 2 edition (February 13, 2007)
- Language: English
- ISBN-10: 1841845183
- ISBN-13: 978-1841845180
- Product Dimensions: 11.4 x 8.8 x 1.2 inches