Reduced cerebrovascular reactivity in posterior cerebral arteries in patients with primary open-angle glaucoma.

PURPOSE: To evaluate the hemodynamics and vasoreactivity in the posterior cerebral artery (PCA) in patients with primary open-angle glaucoma (POAG).

DESIGN: Case-control study.

PARTICIPANTS: Thirteen POAG patients (age range, 40-60 years) with marked visual field loss (mean deviation [MD], <-6 dB); a preserved, mostly normal, central visual field of at least 5°; and best-corrected visual acuity of at least 20/40 formed the study group. Exclusion criterion was presence or history of any systemic disorder including cardiovascular diseases. The control group consisted of 12 healthy subjects matched for age and sex with the study group.

METHODS: Applying transcranial Doppler sonography, we measured hemodynamic parameters in both PCAs at baseline, under monocular reversing checkerboard stimulation, and under hyperventilation. The eye with more marked visual field loss was selected in glaucoma patients, whereas in controls, the tested eye was chosen randomly. Ipsilateral and contralateral PCA were defined according to the tested eye.

MAIN OUTCOME MEASURES: Peak systolic velocity (PSV), end-diastolic velocity, mean velocity (MV), MV change percentage (MV%), resistivity index (RI), pulsatility index (PI).

RESULTS: At baseline, RI (0.55 ± 0.04 vs. 0.52 ± 0.03; P = 0.04) and PI (0.88 ± 0.11 vs. 0.80 ± 0.07; P = 0.04) in the ipsilateral PCA were significantly higher in glaucoma patients than in controls. During checkerboard stimulation, MV% in both PCAs were significantly smaller in the glaucoma group than in controls (19.7 ± 7.2% and 19.0 ± 8.3% vs. 30.7 ± 7.9% and 27.5±9.0%, respectively; P = 0.001 and 0.02, respectively). During hyperventilation, glaucoma patients showed significantly lower MV% in the contralateral PCA than control subjects (-39.8 ± 9.6% versus -47.4 ± 7.0%; P = 0.03). Perimetric pattern standard deviation (PSD) in the tested eye was correlated significantly with RI and PI of the ipsilateral PCA during checkerboard stimulation (P = 0.003, r = -0.76; and P = 0.002, r = -0.76). The MV% of contralateral PCA was correlated inversely with PSD in the fellow eye (P = 0.02, r = -0.64). The difference in MV% between both PCAs was correlated positively with the difference in MD between 2 eyes (P = 0.003, r = 0.75). Under hyperventilation, PSV in the contralateral PCA was correlated negatively with the PSD in the fellow eye (P = 0.03, r = -0.60).

CONCLUSIONS: Vascular insufficiency in the PCAs may be associated with POAG. Changes in the vasoreactivity of PCAs to central visual stimulation may precede marked central visual field loss.