Delayed functional loss in glaucoma. LII Edward Jackson Memorial Lecture.
OBJECTIVE
This study is a systematic exploration of why some patients with glaucoma continue to lose visual field long after therapeutic normalization of their increased intraocular pressures.


METHODS
Three cases of glaucoma are described that had increased intraocular pressures and good initial visual fields.


RESULTS
The following four hypotheses are offered to explain delayed functional loss in these patients: (1) A process independent of intraocular pressure is killing ganglion cells. (2) Unmeasured increases of pressure are killing ganglion cells. (3) The ganglion cells have a genetically determined hypersensitivity to intraocular pressure. (4) The ganglion cells have been rendered hypersensitive to intraocular pressure by irreversible damaging effects of previously increased intraocular pressures


CONCLUSIONS
The current state of knowledge does not permit the elimination of any of the four hypotheses. An additional hypothesis is that the final stage of ganglion cell death is mediated by apoptosis. If so, a potential new treatment for glaucoma would be to inhibit the apoptotic pathway.
Brubaker
R F
RF
Department of Ophthalmology, Mayo Clinic and Mayo Foundation, Rochester, MN 55905, USA.
D000328:Adult; D017209:Apoptosis; D001363:Awards and Prizes; D016923:Cell Death; D005260:Female; D005901:Glaucoma / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D007429:Intraocular Pressure; D008297:Male; D008875:Middle Aged; D009885:Ophthalmology; D012165:Retinal Ganglion Cells / Q000473:pathology; D012955:Societies, Medical; D014786:Vision Disorders / Q000503:physiopathology*; D014794:Visual Fields / Q000502:physiology*