COLOR DOPPLER ANALYSIS OF OCULAR VESSEL BLOOD VELOCITY IN NORMAL-TENSION GLAUCOMA

The pathogenesis of normal-tension glaucoma remains unknown. Because o cular vasospasm has been proposed as a possible mechanism, we investig ated ocular vessel now velocity in normal-tension glaucoma patients at rest and under treatment with a cerebral vasodilator. Ten normal-tens ion glaucoma patients and nine age- and gender-matched controls had no w velocity measured in three vessels (ophthalmic artery, central retin al artery, and temporal short posterior ciliary artery) by using color Doppler imaging, under baseline conditions and during carbon dioxide supplementation sufficient to increase end-tidal PCO2 by 15%. Peak sys tolic and end-diastolic velocities were measured, and the resistance i ndex (peak systolic velocity minus end-diastolic velocity, divided by peak systolic velocity) was calculated. Compared with controls, these normal-tension glaucoma patients had significantly lower end-diastolic velocities (P = .002) and higher resistance indices (P = .007) in the ophthalmic artery at baseline. When PCO2 was increased, control subje cts remained unchanged, whereas it increased end-diastolic velocity in patients (P = .003) and abolished the difference in resistance index between the two groups. Patients and control subjects differed little in their baseline or carbon dioxide response velocities or in resistan ce in the other two vessels. These results indicate that at baseline t hese normal-tension glaucoma patients may have increased vascular resi stance distal to the ophthalmic artery, although this increased resist ance cannot be specifically ascribed to the central retinal arterial o r to temporal short posterior ciliary arterial vascular beds. The resp onsiveness of these patients to a cerebral vasodilator (increased PCO2 ) indicates further that the increased resistance distal to the ophtha lmic artery may be the reversible result of vasospasm.