A 58-year-old man presents to the ophthalmology clinic with progressive loss of peripheral vision over 6 months, initially noticed in the superior temporal quadrant bilaterally. He reports no pain, photopsia, or floaters. Visual acuity is 6/6 in both eyes. Fundoscopy reveals optic disc cupping with a cup-to-disc ratio of 0.8 bilaterally, and intraocular pressure is 28 mmHg in both eyes. Visual field testing confirms superior arcuate defects. What is the primary mechanism of visual loss in this patient?

Explanation

## Pathophysiology of Glaucomatous Optic Neuropathy **Key Point:** Elevated intraocular pressure (IOP) causes mechanical compression and ischemic injury to retinal ganglion cells (RGCs) at the optic nerve head, leading to selective loss of axons and progressive optic nerve atrophy. ### Mechanism of RGC Loss The optic nerve head is the site of maximum vulnerability because: 1. The lamina cribrosa acts as a structural bottleneck where axons are most susceptible to compression 2. Elevated IOP increases extracellular pressure, compromising axoplasmic flow 3. Ischemia develops due to vascular compression and impaired perfusion pressure 4. Excitotoxicity and oxidative stress trigger apoptosis of RGCs ### Clinical Correlation with Visual Field Defects | Feature | Explanation | |---------|-------------| | **Superior arcuate defect** | Damage to superior nasal nerve fibres (arcuate bundle) — earliest sign in glaucoma | | **Peripheral-to-central progression** | RGCs in peripheral retina are damaged first; central vision preserved until late stages | | **Optic disc cupping** | Selective loss of neural tissue at the disc margin, enlarging the cup | | **Normal visual acuity until late** | Central photoreceptors and macular RGCs spared until advanced disease | **Clinical Pearl:** The arcuate (Bjerrum) scotoma is pathognomonic for glaucoma and corresponds to damage of the nerve fibre layer in the distribution of the superior or inferior arcuate bundles. **High-Yield:** Glaucoma is a **selective RGC neuropathy** — photoreceptors and other retinal layers remain intact, explaining why visual acuity is preserved until very late stages despite significant visual field loss. ### Why IOP Matters The relationship between IOP and RGC damage is not strictly linear — individual susceptibility varies, but sustained elevation accelerates axonal loss. The optic nerve head has limited collateral circulation, making it uniquely vulnerable to pressure-induced ischemia. [cite:Aulhorn & Karmeyer, Glaucoma pathophysiology; Harrison 21e Ch 397]