Neuroprotection for treatment of glaucoma in adults.
BACKGROUND
Glaucoma is a heterogeneous group of conditions involving progressive damage to the optic nerve, deterioration of retinal ganglion cells and ultimately visual field loss. It is a leading cause of blindness worldwide. Open angle glaucoma (OAG), the commonest form of glaucoma, is a chronic condition that may or may not present with increased intraocular pressure (IOP). Neuroprotection for glaucoma refers to any intervention intended to prevent optic nerve damage or cell death. The treatment can target extracellular factors such as reducing IOP, or cellular factors derived from the optic nerve itself such as blocking intracellular death signals.


OBJECTIVE
The objective of this review was to systematically examine the evidence regarding the effectiveness of neuroprotective agents, either topical or oral, for slowing the progression of OAG in adults.


METHODS
We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (which contains the Cochrane Eyes and Vision Group Trials Register) (The Cochrane Library, Issue 4, 2009), MEDLINE (January 1960 to January 2010), EMBASE (January 1980 to January 2010), Latin American and Caribbean Literature on Health Sciences (LILACS) (January 1982 to January 2010) and ClinicalTrials.gov (http://clinicaltrials.gov). (5 January 2010). There were no language or date restrictions in the search for trials. The electronic databases were last searched on 5 January 2010.


METHODS
This review was limited to randomized controlled trials (RCTs) in which topical or oral treatments were used to prevent retinal ganglion cell death. Our population of interest was adults with OAG. As the primary outcome for this review was the proportion of participants who developed any progression of visual field loss at five years post intervention, only trials with at least five years of follow-up were included.


METHODS
Two review authors independently reviewed titles and abstracts from the literature searches. Full text copies of relevant or potentially relevant studies were obtained and re-evaluated for inclusion. There were no trials identified for this review, thus we performed no data extraction or meta-analysis. Two studies comparing memantine to placebo are currently awaiting classification until additional study details are provided. Reasons for excluding studies from the review were documented.


RESULTS
In accordance with the selection criteria for inclusion, we identified no studies relevant for this review. The results of short-term trials and other studies are discussed in this review.


CONCLUSIONS
Although neuroprotective agents are intended to act as pharmacological antagonists to prevent cell death, the evidence that they are effective in preventing retinal ganglion cell death, and thus preserving vision in patients with OAG, has not been demonstrated. Long-term RCTs are needed to determine whether or not neuroprotective agents may be beneficial for individuals with OAG.
Sena
Dayse F
DF
Massachusetts Eye and Ear Infirmary, 243 Charles St, Connecting Building 703, Boston, Massachusetts, USA, 02114.
Ramchand
Kanchan
K
Lindsley
Kristina
K
D000284:Administration, Oral; D000287:Administration, Topical; D000328:Adult; D016923:Cell Death; D018450:Disease Progression; D005902:Glaucoma, Open-Angle / Q000188:drug therapy*; D006801:Humans; D018696:Neuroprotective Agents / Q000008:administration & dosage*; D009900:Optic Nerve; D009901:Optic Nerve Diseases / Q000209:etiology / Q000517:prevention & control*; D012165:Retinal Ganglion Cells / Q000502:physiology
D018696:Neuroprotective Agents