What Is the Present Pathogenetic Concept of Glaucomatous Optic Neuropathy?
Section snippets
Glaucomatous Optic Neuropathy
Glaucomatous optic neuropathy (GON) comprises of the following mutually dependant basic components: loss of neural tissue, activation of glial cells, tissue remodeling, change of blood flow.
Risk Factors for Glaucoma
Factors associated with an increase of IOP are not the same as factors associated with the development of GON. Furthermore, factors related to either IOP increase or to damage may not automatically be causal.
Ocular Blood Flow and Glaucomatous Optic Neuropathy
Whether OBF plays a role in the pathogenesis of GON has often been discussed in the past. For decades the literature remained controversial.
The Pathogenetic Concept of GON
Among others, there are two major pathogenetic components: damage to the axons and the activation of the astrocytes (Fig. 4).
Mechanical stress (e.g., by an increase in IOP) activates astrocytes by stimulating the epidermal growth factor receptor (EGFR).71 Astrocytes, however, are also activated by endothelin, which is upregulated as a consequence of cell stress—for example, by RI.
The major insult to the axons is brought about by RI, which is the consequence of an unstable oxygen supply (due to
Method of Literature Search
A systematic search of the Medline database using the PubMed Web site for the years 1966 through January 2007 was conducted using the following key words: POAG, pathogenesis, glaucoma, vasospasm, vascular dysregulation, autoregulation, ischemia, endothelin, glaucomatous optic neuropathy, glial cells, tissue remodeling, ocular blood flow, risk factors, trabecular meshwork, primary vascular dysregulation, nitric oxide synthase, secondary vascular dysregulation, reperfusion damage, oxidative
References (133)
- et al.
The eye in sleep apnea syndrome
Sleep Med
(2006) - et al.
Factors that predict the benefit of lowering intraocular pressure in normal tension glaucoma
Am J Ophthalmol
(2003) - et al.
Racial heterogeneity in coronary artery vasomotor reactivity: differences between Japanese and Caucasian patients
J Am Coll Cardiol
(1999) - et al.
Central corneal thickness and measured IOP response to topical ocular hypotensive medication in the Ocular Hypertension Treatment Study
Am J Ophthalmol
(2004) - et al.
Deficiency in matrix metalloproteinase gelatinase B (MMP-9) protects against retinal ganglion cell death after optic nerve ligation
J Biol Chem
(2002) The vascular concept of glaucoma
Surv Ophthalmol
(1994)- et al.
The impact of ocular blood flow in glaucoma
Prog Retin Eye Res
(2002) - et al.
Vasospasm, its role in the pathogenesis of diseases with particular reference to the eye
Prog Retin Eye Res
(2001) - et al.
Blood-cell velocity in the nailfold capillaries of patients with normal-tension and high-tension glaucoma
Am J Ophthalmol
(1991) - et al.
Relationship between ocular perfusion pressure and retrobulbar blood flow in patients with glaucoma with progressive damage
Am J Ophthalmol
(2000)
What are the biomarkers for glaucoma?
Surv Ophthalmol
Ambulatory blood pressure monitoring in glaucoma. The nocturnal dip
Ophthalmology
Chronic ocular hypertension induces dendrite pathology in the lateral geniculate nucleus of the brain
Exp Eye Res
Potential role of nitric oxide and endothelin in the pathogenesis of glaucoma
Surv Ophthalmol
Blood-flow velocities of the extraocular vessels in patients with high-tension and normal-tension primary open-angle glaucoma
Am J Ophthalmol
Optic disc hemorrhage in low-tension glaucoma
Ophthalmology
Interim clinical outcomes in the Collaborative Initial Glaucoma Treatment Study comparing initial treatment randomized to medications or surgery
Ophthalmology
Oxidative injury by peroxynitrite in neural and vascular tissue of the lateral geniculate nucleus in experimental glaucoma
Exp Eye Res
Choroidal innervation in primate eyes
Exp Eye Res
High prevalence of glaucoma in patients with sleep apnea syndrome
Ophthalmology
Is there more to glaucoma treatment than lowering IOP?
Surv Ophthalmol
Color Doppler imaging in patients with asymmetric glaucoma and unilateral visual field loss
Am J Ophthalmol
A sick eye in a sick body? Systemic findings in patients with primary open-angle glaucoma
Surv Ophthalmol
Cold feet and prolonged sleep-onset latency in vasospastic syndrome
Lancet
Choroidal capillary and venous congestion in central serous chorioretinopathy
Am J Ophthalmol
Expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases in human optic nerve head astrocytes
Glia
Choroidal innervation and optic neuropathy in macacque monkeys with laser- or anterior chamber perfusion-induced short-term elevation of intraocular pressure
Exp Eye Res
Histochemical localisation of mitochondrial enzyme activity in human optic nerve and retina
Br J Ophthalmol
Large diurnal fluctuations in intraocular pressure are an independent risk factor in patients with glaucoma
J Glaucoma
Corneal thickness in glaucoma screening, diagnosis, and management
Curr Opin Ophthalmol
Ambulatory blood pressure monitoring in glaucoma patients. The nocturnal systolic dip and its relationship with disease progression
Int Ophthalmol
Neuronal thread protein gene modulation with cerebral infarction
J Cereb Blood Flow Metab
Do patients with low tension glaucoma have particular cardiovascular characteristics?
Ophthalmologica
Central corneal thickness and vascular risk factors in normal tension glaucoma
Acta Ophthalmol Scand
The visual field of low tension glaucoma and shock-induced optic neuropathy
Arch Ophthalmol
Shock-induced optic neuropathy: a cause of nonprogressive glaucoma
N Engl J Med
[Visual fields changes in chronic angle closure glaucoma patients after their intraocular pressures were well controlled]
Zhongguo Yi Xue Ke Xue Yuan Xue Bao
Increased plasma endothelin-1 levels in patients with progressive open angle glaucoma
Br J Ophthalmol
[Glaucomatous optic neuropathy: a reperfusion injury]
Klin Monatsbl Augenheilkd
[Quantitative perimetry in the glaucoma patient without local visual field defects]
Graefes Arch Clin Exp Ophthalmol
Do ocular vasospasms help cause normal tension glaucoma?
Doc Ophthalmol Proc Series
Vascular dysregulation: a principal risk factor for glaucomatous damage?
J Glaucoma
Susac syndrome: a vasospastic disorder?
Eur J Ophthalmol
[Comparison of the effectiveness and safety of levobunolol and timolol in ocular hypertension and chronic open-angle glaucoma]
Klin Monatsbl Augenheilkd
Regression of capillary network in atrophied soleus muscle induced by hindlimb unweighting
J Appl Physiol
Ocular hemodynamics and glaucoma prognosis: a color Doppler imaging study
Arch Ophthalmol
Finger microcirculation in classical migraine. A video-microscopic study of nailfold capillaries
Eur Neurol
Body mass index in glaucoma
J Glaucoma
Is vascular regulation in the central retinal artery altered in persons with vasospasm?
Arch Ophthalmol
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