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Updated: Aug 6, 2026

Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments
Published on: April 24, 2020
Compromised autoregulatory control of ocular hemodynamics in glaucoma patients after postural change
Peter Galambos1, Joanna Vafiadis, Silvia E Vilchez
1Glaukomlabor, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Purpose:
The autoregulatory control of retrobulbar blood flow in response to postural challenge was investigated in normal-tension glaucoma (NTG) patients in comparison with primary open-angle glaucoma (POAG) patients and healthy volunteers.
Design:
Prospective cohort study.
Participants And Controls:
Twenty POAG patients, 20 NTG patients, and 20 control subjects.
Methods:
Peak systolic velocity (PSV), end diastolic velocity (EDV), and resistivity index (RI) in the short posterior ciliary artery (SPCA), central retinal artery (CRA) and ophthalmic artery (OA) were recorded after a change from sitting upright to a supine body position using color Doppler imaging.
Main Outcome Measures:
Peak systolic velocity, EDV, and RI.
Results:
Ten minutes after postural change to a supine position, blood flow velocities in the SPCA remained unchanged in controls, whereas a significant increase of PSV and EDV was found in both glaucoma groups. The RI in the SPCA was significantly lowered in the NTG group. Recordings for the OA and CRA showed a significant increase in EDV and significant decrease in RI in all 3 groups; a significant increase in PSV in the CRA was detected only in the NTG group.
Conclusions:
The unaltered flow velocities in the SPCA of healthy controls may indicate tight autoregulatory control, whereas the flow velocities in the CRA and OA appeared to follow alterations in hydrostatic pressure. In contrast, NTG and POAG patients demonstrated an insufficient compensatory response to postural change, leading to accelerated flow in the SPCA. This compromised autoregulatory control could represent another contributing factor in the pathogenesis of glaucoma.
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