Ignite Creation Date:
2024-05-05 @ 4:47 PM
Last Modification Date:
2024-10-26 @ 9:24 AM
Study NCT ID:
NCT00317577
Status:
COMPLETED
Last Update Posted:
2006-04-25
First Post:
2006-04-23
Brief Title:
Study of Medical Treatment of Low-Pressure Normal Tension Glaucoma
Sponsor:
Chicago Center for Vision Research
Organization:
Chicago Center for Vision Research
Study Overview
Official Title:
A Multicenter Double-Masked 2-Arm Parallel Group Study Comparing the Effect of Brimonidine 02 Versus Timolol 05 on Visual Field Stability in Patients With Low-Pressure Glaucoma
Status:
COMPLETED
Status Verified Date:
2006-04
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Low-pressure normal tension glaucoma is a type of open-angle glaucoma resulting in damage to the optic nerve and abnormalities of the visual field Eye intraocular pressure in this type of glaucoma is not higher than that usually considered to be normal less than 21 mmHg for the eye The present treatment of low-pressure glaucoma is also directed to lowering the normal eye pressure Both medications in this study brimonidine and timolol lower eye pressure
Laboratory research over the past decade indicates the potential to treat glaucoma not only by lowering eye pressure but with treatments aimed at the damage occurring at the optic nerve One group of drugs selective alpha2-adrenergic agonists have been shown in laboratory animals to protect against the effects of nerve damage following local stroke Brimonidine one of the medications in the current study is a selective alpha2-adrenergic agonist which protects against damage to optic nerve in animal models of glaucoma
The hypothesis of the present study is that brimonidine eye drops provide protection to the damaged optic nerve independent of lowering eye pressure in patients with low-pressure glaucoma This will be determined by 1 measuring eye pressure 2 performing visual field examinations and 3 examination of the optic nerve
Laboratory research over the past decade indicates the potential to treat glaucoma not only by lowering eye pressure but with treatments aimed at the damage occurring at the optic nerve One group of drugs selective alpha2-adrenergic agonists have been shown in laboratory animals to protect against the effects of nerve damage following local stroke Brimonidine one of the medications in the current study is a selective alpha2-adrenergic agonist which protects against damage to optic nerve in animal models of glaucoma
The hypothesis of the present study is that brimonidine eye drops provide protection to the damaged optic nerve independent of lowering eye pressure in patients with low-pressure glaucoma This will be determined by 1 measuring eye pressure 2 performing visual field examinations and 3 examination of the optic nerve
Detailed Description:
The term glaucoma describes a specific pattern of optic nerve head and visual field damage caused by a number of different diseases of the eye most but not all of which are associated with an elevated eye pressure Glaucoma is currently considered to be a progressive neurodegenerative disorder Low-pressure glaucoma LPG is a type of open-angle glaucoma OAG with progressive visual field and optic nerve damage despite an untreated eye pressure in the statistically normal mean 159 SD 29 mmHg range usually less than 21 mmHg Therefore in this condition pressure-independent mechanisms eg vascular or structural defects of the optic nerve may be the main if not the sole cause of the optic neuropathy LPG represents 67 to 683 of all OAGs
Current glaucoma treatment is directed to lowering eye pressure using medical therapy eye drops laser treatment andor surgery to a level that stops progressive optic nerve damage The efficacy of lowering eye pressure in LPG has been reported Both protocol medical treatments brimonidine and timolol show similar efficacy to lower eye pressure
Laboratory research over the past decade indicates the potential to manage glaucoma not only by lowering eye pressure but with treatment modalities aimed at the damage occurring at the optic nerve Possible therapies may include agents effective as neuronal protectants to increase or prolong the survival rate of injured retinal ganglion cells Treatments could also be directed to the rescue of nerve fibers from secondary degeneration as stimulants to expand dendritic fields and to promote nerve regeneration or neural transplantation
Selective α2-adrenergic agonists have been shown to have a neuroprotective effect in animal models of focal cerebral ischemia Brimonidine is reported to protect the optic nerve and retinal ganglion cells from secondary degeneration following a partial crush lesion to the adult rat optic nerve One molecular mechanism for this neuroprotection may relate to up-regulation of neuronal survival factors In rats systemic α2-adrenergic agonists induce basic fibroblast growth factor mRNA in the retina Treatment with α2-agonists before and during constant light exposure reduces retinal photoreceptor degeneration in albino rats Animal studies demonstrate that topical administration of brimonidine results in pharmacologic concentrations of drug in the vitreous 100-170 nM Therefore ocular dosing with brimonidine provides a route for drug delivery to the retina in amounts sufficient to bind and activate the α2-adrenoceptor and provide a neuroprotective effect
The study hypothesis is to evaluate the ability of topical treatment with 02 brimonidine a highly selective α2-adrenergic agonist to impart neuroprotection to the damaged optic nerve in patients with LPG Comparison is made to 05 timolol a nonselective β-adrenergic antagonist without reported neuroprotective properties Patients will be randomly assigned to twice daily double-masked treatment with one of these drugs Neuroprotection will be assessed by evaluation of automated static visual fields performed at 4 month intervals for 4 years of treatment
Current glaucoma treatment is directed to lowering eye pressure using medical therapy eye drops laser treatment andor surgery to a level that stops progressive optic nerve damage The efficacy of lowering eye pressure in LPG has been reported Both protocol medical treatments brimonidine and timolol show similar efficacy to lower eye pressure
Laboratory research over the past decade indicates the potential to manage glaucoma not only by lowering eye pressure but with treatment modalities aimed at the damage occurring at the optic nerve Possible therapies may include agents effective as neuronal protectants to increase or prolong the survival rate of injured retinal ganglion cells Treatments could also be directed to the rescue of nerve fibers from secondary degeneration as stimulants to expand dendritic fields and to promote nerve regeneration or neural transplantation
Selective α2-adrenergic agonists have been shown to have a neuroprotective effect in animal models of focal cerebral ischemia Brimonidine is reported to protect the optic nerve and retinal ganglion cells from secondary degeneration following a partial crush lesion to the adult rat optic nerve One molecular mechanism for this neuroprotection may relate to up-regulation of neuronal survival factors In rats systemic α2-adrenergic agonists induce basic fibroblast growth factor mRNA in the retina Treatment with α2-agonists before and during constant light exposure reduces retinal photoreceptor degeneration in albino rats Animal studies demonstrate that topical administration of brimonidine results in pharmacologic concentrations of drug in the vitreous 100-170 nM Therefore ocular dosing with brimonidine provides a route for drug delivery to the retina in amounts sufficient to bind and activate the α2-adrenoceptor and provide a neuroprotective effect
The study hypothesis is to evaluate the ability of topical treatment with 02 brimonidine a highly selective α2-adrenergic agonist to impart neuroprotection to the damaged optic nerve in patients with LPG Comparison is made to 05 timolol a nonselective β-adrenergic antagonist without reported neuroprotective properties Patients will be randomly assigned to twice daily double-masked treatment with one of these drugs Neuroprotection will be assessed by evaluation of automated static visual fields performed at 4 month intervals for 4 years of treatment
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None