BACKGROUND: Several studies suggest that nocturnal reductions in systemic blood pressure (BP) may be associated with onset or progression of glaucomatous optic neuropathy. The present study aimed to find out whether reductions in nocturnal BP are linked to retrobulbar blood flow perturbations in glaucoma patients. METHODS: Fifteen patients with non-progressing glaucoma and 15 controls were studied in the evening ("baseline") and then at a point of significantly reduced arterial BP during the night. Flow velocities were measured with color Doppler imaging (CDI) in the ophthalmic, central retinal, and nasal and temporal short posterior ciliary arteries, and with transcranial Doppler (TCD) in the middle cerebral artery. BP, corrected for posture, was monitored throughout the night. RESULTS: Maximal posture-corrected nocturnal BP reductions were similar in patients and controls. The reductions were about 10% for each group ( P<0.01). At baseline, patients had lower peak systolic and end-diastolic velocity ( P<0.05) in the short posterior ciliary arteries than controls. Flow velocities in these arteries remained constant in glaucoma patients, while controls showed significant declines. Patients and controls demonstrated blood flow velocities unchanged from baseline in the central retinal, ophthalmic, and middle cerebral arteries during nocturnal BP reduction. CONCLUSIONS: In patients with non-progressing glaucoma there was no evidence of cerebral or retrobulbar hemodynamic abnormalities during nocturnal BP dips. Posterior ciliary arterial blood flow velocities were similar in glaucoma patients and controls during nocturnal BP dips.
BACKGROUND: Several studies suggest that nocturnal reductions in systemic blood pressure (BP) may be associated with onset or progression of glaucomatous optic neuropathy. The present study aimed to find out whether reductions in nocturnal BP are linked to retrobulbar blood flow perturbations in glaucomapatients. METHODS: Fifteen patients with non-progressing glaucoma and 15 controls were studied in the evening ("baseline") and then at a point of significantly reduced arterial BP during the night. Flow velocities were measured with color Doppler imaging (CDI) in the ophthalmic, central retinal, and nasal and temporal short posterior ciliary arteries, and with transcranial Doppler (TCD) in the middle cerebral artery. BP, corrected for posture, was monitored throughout the night. RESULTS: Maximal posture-corrected nocturnal BP reductions were similar in patients and controls. The reductions were about 10% for each group ( P<0.01). At baseline, patients had lower peak systolic and end-diastolic velocity ( P<0.05) in the short posterior ciliary arteries than controls. Flow velocities in these arteries remained constant in glaucomapatients, while controls showed significant declines. Patients and controls demonstrated blood flow velocities unchanged from baseline in the central retinal, ophthalmic, and middle cerebral arteries during nocturnal BP reduction. CONCLUSIONS: In patients with non-progressing glaucoma there was no evidence of cerebral or retrobulbar hemodynamic abnormalities during nocturnal BP dips. Posterior ciliary arterial blood flow velocities were similar in glaucomapatients and controls during nocturnal BP dips.