Effect of brimonidine on retinal vascular autoregulation and short-term visual function in normal tension glaucoma.
OBJECTIVE
To assess whether brimonidine 0.15% alters retinal vascular autoregulation and short-term visual function in normal tension glaucoma patients who demonstrate retinal vascular dysregulation.


METHODS
Nonrandomized clinical trial.


METHODS
In this prospective study, 46 normal tension glaucoma patients not previously treated with brimonidine underwent retinal vascular autoregulation testing and visual function assessment using frequency doubling technology perimetry and equivalent noise motion sensitivity testing. We measured blood flow in a major temporal retinal artery with subjects seated and then while reclined for 30 minutes. Patients having a change in retinal blood flow with posture change outside the range previously found in healthy subjects were classified as having retinal vascular dysregulation. They were treated with brimonidine 0.15% for 8 weeks and designated for retesting.


RESULTS
Twenty-three patients demonstrated retinal vascular dysregulation at the initial visit. Younger age (P = .050) and diabetes (P = .055) were marginally significant risk factors for retinal vascular dysregulation. After the 8-week course with brimonidine, 14 of the 17 patients who completed the study showed a return of posture-induced retinal blood flow changes to levels consistent with normal retinal vascular autoregulation (P < .0001). We found no significant changes in frequency doubling technology perimetry or in motion detection parameters following treatment with brimondine (P > .09 for all tests performed).


CONCLUSIONS
Brimonidine significantly improved impaired retinal vascular autoregulation in normal tension glaucoma patients, but short-term alteration in visual function could not be demonstrated.
Massachusetts Eye & Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts.
Gilbert T
GT
Feke
Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts.
Peter J
PJ
Bex
Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts.
Christopher P
CP
Taylor
Massachusetts Eye & Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts.
Douglas J
DJ
Rhee
Massachusetts Eye & Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts.
Angela V
AV
Turalba
Massachusetts Eye & Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts.
Teresa C
TC
Chen
Consulting Ophthalmologists, Farmington, Connecticut.
Martin
M
Wand
Massachusetts Eye & Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts. Electronic address: Louis_Pasquale@meei.harvard.edu.
Louis R
LR
Pasquale
D058647:Adrenergic alpha-2 Receptor Agonists / Q000627:therapeutic use*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001783:Blood Flow Velocity; D000068438:Brimonidine Tartrate; D005260:Female; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D007429:Intraocular Pressure / Q000502:physiology; D057066:Low Tension Glaucoma / Q000188:drug therapy* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009883:Ophthalmic Solutions; D011187:Posture; D011446:Prospective Studies; D011810:Quinoxalines / Q000627:therapeutic use*; D012171:Retinal Vessels / Q000503:physiopathology*; D014792:Visual Acuity / Q000502:physiology*; D058609:Visual Field Tests; D014794:Visual Fields / Q000502:physiology
D058647:Adrenergic alpha-2 Receptor Agonists; D009883:Ophthalmic Solutions; D011810:Quinoxalines; D000068438:Brimonidine Tartrate