Low-Pressure Glaucoma Biomechanics & Perfusion Simulator

Pathology Presets Clinical Scenarios

Biomechanical Sliders

Intraocular Pressure (IOP) 15.0 mmHg

Vitreous fluid hydrostatic pressure pushing posteriorly against optic disc.

Retrobulbar CSF Pressure (ICP) 11.0 mmHg

Subarachnoid space fluid pressure opposing IOP from behind the eye.

Mean Arterial Pressure (MAP) 93.3 mmHg

Systemic BP driver. Nocturnal dipping below 65 mmHg induces severe optic nerve ischemia.

Lamina Cribrosa Compliance Normal (1.0x)

Higher values = thinner, hyper-compliant collagen beams prone to shear deformation.

Intact Axon / BDNF Vesicles

Ischemic / Pinched Axon Bundles

Collagenous Lamina Cribrosa Beams

Retrobulbar CSF Chamber

Optic Disc Microcapillaries

How Glaucoma Occurs When Intraocular Pressure is Statistically "Normal"

In classic High-Tension Glaucoma, elevated eye pressure (>21 mmHg) directly crushes the optic nerve. In Normal-Tension Glaucoma (NTG), intraocular pressure (IOP) registers in the normal range (10–20 mmHg), yet retinal ganglion cells and optic disc axons still progressively die. NTG is driven by two insidious biomechanical and vascular realities:

1. The Translaminar Pressure Gradient (ΔP = IOP − ICP) The lamina cribrosa does not feel IOP alone; it sits between the anterior intraocular space and the posterior retrobulbar CSF space. An abnormally low intracranial/CSF pressure creates an identical destructive shearing gradient (ΔP > 8 mmHg) backward.

2. Nocturnal Hypotension & Perfusion Collapse Ocular Perfusion Pressure is calculated as OPP = ⅔ MAP − IOP. When blood pressure dips during sleep or vasospasm occurs (Flammer syndrome), perfusion drops below critical auto-regulation thresholds (< 40 mmHg), starving laminar capillaries.

3. Focal Lamina Cribrosa Vulnerability NTG optic discs frequently exhibit thinner collagen beams and pore enlargement in superior/inferior poles. Normal forces produce hyper-strain, cutting off orthograde and retrograde axoplasmic transport of brain-derived neurotrophic factor (BDNF).

4. Dense Paracentral Scotomas Because inferior and superior laminar pores suffer the greatest mechanical shear, NTG characteristically damages maculopapillary bundle axons first, creating steep visual field loss right near central vision.

Physiological Telemetry Real-Time

Translaminar Pressure Gradient

+4.0 mmHg ΔP = IOP − ICP

Ocular Perfusion Pressure (OPP)

47.2 mmHg ⅔MAP − IOP

Lamina Cribrosa Deflection Strain

2.8 µm ε = f(ΔP, Compl)

Axonal Transport Efficiency

98% BDNF flux / s

Visual Field Test (24-2 HVF) Paracentral Defect

Normal Visual Field (MD: -0.4 dB)

Dark squares indicate paracentral scotoma progression typical of NTG due to maculopapillary axon loss.

Diagnostic Assessment JSON Export

Active snapshot with mathematical indices, physiological strain tensors, and clinical recommendations.

State Record: