Revelatio™ — From the Latin: "an unveiling; the disclosure of what was previously hidden."
Understanding Glaucoma Beyond Intraocular Pressure.
Intraocular pressure is not glaucoma. It is a risk factor — an important one — but it does not explain why some optic nerves fail at low pressures while others survive at high ones. Slow Breach explores the full landscape of optic nerve vulnerability: vascular insufficiency, structural susceptibility, impaired axonal transport, neuroinflammation, and the emerging science of glymphatic clearance. This is a course about seeing glaucoma as it actually is — a disease of the optic nerve, not merely a disease of pressure.
The clinician who understands optic nerve vulnerability beyond IOP makes better decisions at every stage of glaucoma care — from risk stratification and target pressure selection to the recognition of progression despite controlled pressure. This framework does not replace IOP management. It completes it.
A Note on This Experience
Slow Breach is designed for clinicians who want to understand glaucoma at a deeper level — not to replace their current approach, but to complete it. The goal is not to abandon IOP management, but to see it within a richer clinical and scientific context.
Course Details
Credit hours and COPE approval pending. Join the waitlist to receive notification when this course becomes available.
Upon successful completion of this educational experience, the clinician will be able to:
Articulate the limitations of an IOP-centric model of glaucoma pathogenesis.
Describe the vascular, structural, mechanical, inflammatory, and clearance factors that contribute to optic nerve vulnerability.
Apply a multi-factor vulnerability framework to clinical risk stratification and management decisions.
Recognize clinical presentations and patterns that suggest non-pressure-dependent mechanisms of glaucomatous progression.
Integrate emerging concepts — including glymphatic dysfunction and neuroinflammation — into a comprehensive understanding of glaucoma pathogenesis.
This educational experience is organized into the following modules. Content is subject to refinement prior to final release.
The case for a multi-factor model of glaucoma — what IOP explains, what it does not, and why the distinction matters clinically.
Ocular perfusion pressure, vascular dysregulation, and the role of systemic cardiovascular factors in optic nerve susceptibility.
Lamina cribrosa biomechanics, optic nerve head architecture, and the structural determinants of vulnerability to pressure-related stress.
How impaired axonal transport and inflammatory cascades contribute to retinal ganglion cell loss — the cellular mechanisms of glaucomatous neurodegeneration.
The emerging science of glymphatic dysfunction in glaucoma — what it means for our understanding of disease pathogenesis and potential future therapeutic targets.
Translating the multi-factor vulnerability framework into clinical practice — risk stratification, target pressure selection, and the recognition of pressure-independent progression.
Educational Philosophy
This educational experience is designed to support clinical reasoning and evidence-informed decision-making. It does not constitute clinical advice and should not replace consultation of official prescribing information, applicable standards of care, or the clinical judgment of the treating clinician. COPE approval and credit hours are pending and will be confirmed prior to release.
Join the waitlist for Slow Breach and receive notification when this educational experience becomes available.
Companion Resource
Explore the therapeutic reference library designed to support the clinical reasoning developed in MYODCE educational experiences.
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