Stuart K Gardiner PhD Devers Eye Institute, Discoveries In Sight
Co-authors: Brad Fortune OD PhD Grant Cull BSc Lin Wang MD PhD
Blood flow within the optic nerve head (ONH) decreases in severe glaucoma. However animal studies suggest an increase in flow at the earliest stage of glaucoma. To investigate this further, we used Laser Speckle Flowgraphy (LSFG) to quantify human pulsatile blood flow within ONH capillaries. 4-second LSFG image series are used to generate a mean blur rate (MBR) map representing flow distribution within the ONH. After eliminating large vessels, MBR within the remaining ONH area is averaged into one heartbeat cycle. 93 eyes with functional loss, and 74 glaucoma suspect / fellow eyes without functional loss, were compared against 92 healthy control eyes, after age-correcting parameters using linear regression among the control eyes. The average age-corrected MBR was higher in glaucoma suspect / fellow eyes than control eyes (16.4 vs. 12.5 units, p<0.0001); then lower again in eyes with functional loss (13.8 units). The maximal rate of increase of MBR during the pulsatile cycle was greater for suspect / fellow eyes than control eyes (p<0.0001), but similar between eyes with functional loss and control eyes (p=0.8323). The increase in MBR for suspect / fellow eyes was similar to control eyes within the first 10% of the pulsatile cycle (+3.11 vs. +3.00, p=0.7519); but greater between 10-20% of the cycle (+4.73 vs. +3.94, p=0.0125) and between 20-30% of the cycle (+2.02 vs. +0.89, p<0.0001). These results suggest a reduction in the ability of vessels and/or capillaries to dilate to accommodate peak pulsatile flow volumes, causing an increase in maximal flow velocity. Increased metabolic demand could increase flow volume such that vessels reach their accommodative maximum diameter during the pulsatile cycle. Conversely, biomechanical stiffening of vessel walls could reduce that accommodative maximum diameter. Later in the disease process, blood flow decreases with loss of neural tissue and resultant metabolic demand.
Funding Sources: NEI R01 EY020922; Good Samaritan Foundation
