The acute morphologic changes that occur at the optic nerve head induced by medical reduction of intraocular pressure.
OBJECTIVE
The mechanical theory of glaucoma postulates that raised intraocular pressure (IOP) causes laminar distortion resulting in damage to axons at the optic nerve head. There is some evidence that the change in morphology may occur over a short time course. The aim of this paper was to detail the acute morphologic changes at the optic nerve head when IOP was lowered with medical therapy in a clinical population.


METHODS
Subjects referred to the glaucoma clinic that had a documented IOP of over 28 mm Hg, on no treatment, in one or both eyes were included. Tonometry, pachymetry, and scanning laser ophthalmoscopy were performed before and after lowering IOP with topical apraclonidine and oral acetazolamide. The significance of change in outcome variables was assessed using a paired t test allowing for dependence within subjects and, for sensitivity, with a nonparametric Wilcoxon signed-rank test.


RESULTS
Data were obtained from 38 eyes of 19 patients with a mean age of 67 years. After lowering IOP for only 1 hour, there was a significant decrease in mean cup volume (mean change in volume below surface 26.8 microm3, P< or =0.001) and mean cup depth (13.8 microm, P<0.01), there being a corresponding increase in mean rim area (37.3 microm2, P<0.034). There was no statistically significant change in central corneal thickness after administration of the IOP lowering medications.


CONCLUSIONS
In the present study, it was shown that acute and statistically significant alterations in optic disc morphology occur when IOP is lowered medically with a combination of topical apraclonidine and systemic acetazolamide. The technique, therefore, may be useful to further investigate subgroups of glaucomatous eyes and test etiologic hypotheses.
Meredith
Sarah P
SP
Department of Ophthalmology, Norfolk and Norwich University Hospital, Norwich, UK.
Swift
Louise
L
Eke
Tom
T
Broadway
David C
DC
D000086:Acetazolamide / Q000008:administration & dosage; D000284:Administration, Oral; D000287:Administration, Topical; D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage*; D000368:Aged; D000369:Aged, 80 and over; D002257:Carbonic Anhydrase Inhibitors / Q000008:administration & dosage*; D003000:Clonidine / Q000008:administration & dosage / Q000031:analogs & derivatives; D004359:Drug Therapy, Combination; D005260:Female; D005902:Glaucoma, Open-Angle / Q000188:drug therapy / Q000503:physiopathology; D006801:Humans; D007429:Intraocular Pressure / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D009887:Ophthalmoscopy; D009898:Optic Disk / Q000473:pathology*; D009901:Optic Nerve Diseases / Q000188:drug therapy / Q000503:physiopathology; D014065:Tonometry, Ocular
D000316:Adrenergic alpha-Agonists; D002257:Carbonic Anhydrase Inhibitors; C016986:apraclonidine; D003000:Clonidine; D000086:Acetazolamide