Glaucoma Progression: From Optic Neuropathy to Blindness

Glaucoma is a group of optic neuropathies characterized by progressive retinal ganglion cell (RGC) death and corresponding visual field loss. Elevated intraocular pressure (IOP) is the major modifiable risk factor, but normal‑tension glaucoma (NTG) occurs with IOP ≤21 mmHg.

Pathophysiology

• Mechanical stress at lamina cribrosa → axonal transport blockade.
• Vascular dysregulation → ischemic injury to optic nerve head.
• Neuroinflammation, excitotoxicity, mitochondrial dysfunction, apoptosis.

Clinical Course

1. Pre‑perimetric: Structural loss (RNFL thinning on OCT, optic disc cupping) before visual field defect.
2. Early field loss: Nasal step, arcuate scotoma, paracentral defect (superior/inferior).
3. Moderate/advanced: Coalescing defects, temporal island, central preservation until late.
4. End‑stage: Tunnel vision → no light perception.

Progression Rate

• Untreated: Mean deviation (MD) worsens ~0.5–1 dB/yr (highly variable).
• Treated (IOP reduction 20–30%): Slows by ~50%; some still progress.
• Risk factors for fast progression: high peak IOP, thin CCT, disc hemorrhage, older age, vascular dysregulation, poor adherence.

Treatment

• First‑line: Prostaglandin analogs (latanoprost, travoprost, bimatoprost, tafluprost) — once nightly, 25–35% IOP reduction.
• Add‑ons: β‑blockers, α₂‑agonists, carbonic anhydrase inhibitors, Rho kinase inhibitors (netarsudil).
• Laser: SLT (first‑line alternative), ALT, MLT, micropulse cyclophotocoagulation.
• Surgery: Trabeculectomy, tube shunt, MIGS (iStent, Hydrus, Xen) for mild‑moderate.

Monitoring

IOP q3–6 mo; OCT RNFL/GCC annually; visual fields q6–12 mo. Target IOP individualized (typically 20–30% below baseline).

Early detection via comprehensive eye exam (tonometry, gonioscopy, optic nerve, OCT, VF) preserves vision.