How dynamic pulsatile mechanisms determine aqueous outflow.
This is an important 2013 article by Murray Johnstone, MD, describing his ground-breaking research in glaucoma.
I have been doing my best to raise awareness of Dr. Johnstone's work for the last ten years, but many of us (whether professional or layperson) are still not familiar with this important new understanding. I continue to see glaucoma papers published in major journals where the authors refer to the outdated notion of passive drainage and/or restate the incorrect idea that 75% of the resistance to aqueous outflow is located in the trabecular meshwork (TM). (I'm currently looking at a peer reviewed paper with a 2023 publication date that appears confused on this topic.)
This related video really helps in understanding these concepts:
Trabecular Meshwork Pulse-induced Motion Video http://youtu.be/51MheK88170
The ocular pulse is driven by the heart beat. The video shows the pulsatile action of the trabecular meshwork and Schlemm's canal in action.
Here is the introduction from Dr. Johnstone's important 2013 article:
The traditional glaucoma model is predicated on evidence from microsurgical studies that date to the middle of the last century1 The model became entrenched in the literature but does not conform to findings from a later, more complete body of evidence by the same author and his colleagues. 2-5 The midcentury studies led to the following series of premises based on indirect evidence and assumptions:
- Seventy-five percent of the resistance to aqueous outflow is located in the trabecular meshwork (TM)
- The site of resistance is in a geometrically stable juxtacanalicular space
- Extracellular matrix in the juxtacanalicular space, acting as a passive filter, controls the flow of aqueous humor
- Aqueous humor flow itself is passive
- The TM does not move in vivo
Grant, who performed the studies from which these initial premises were developed1 eventually published studies along with colleagues that challenged his earlier conclusions.2-5 The later research suggested that
- Approximately 25% of resistance can be attributed to the TM, about 25% to the distal outflow pathways, and approximately 50% to apposition between the walls of Schlemm canal (SC)2,3
- The juxtacanalicular space cannot act as a stable passive filter. First, it does not have enough extracellular matrix material to do so. Second, it enlarges up to 300% as the IOP rises within a physiologic range. Third, biomechanical studies have demonstrated that SC inner-wall endothelium is the primary tissue layer undergoing deformation in response to an increase in pressure4,5
- The TM's distension into SC causes the canal's walls to become appositional at nearly physiologic pressures, creating resistance by preventing aqueous access to collector channels.4,5
- Pulsatile aqueous flow from SC into the aqueous veins provides direct evidence that aqueous flow is not passive but rather the result of dynamic phenomena6 (Figure 1)
- Pulse-dependent motion of the TM accounts for aqueous outflow, as shown by recent phasesensitive optical coherence tomography (PhS-OCT) studies (Figure 2) in ex vivo primate eyes7 and in human eyes8
Continue reading at Glaucoma Today