Addicks E M

Quigley H A, Hohman R M, Addicks E M, Green W R

Glaucoma research in primates and humans found optic disc capillary density remains proportional to tissue loss, not selectively reduced. This suggests blood supply isn't the primary cause of neural damage.

Quigley H A, Hohman R M, Addicks E M, Massof R W, Green W R

Studying glaucomatous eyes, researchers found early lamina cribrosa compression, even before visual field loss, suggesting mechanical stress is a primary driver of optic nerve damage.

Quigley H A, Hohman R M, Addicks E M

Studying primate optic disks, researchers found optic disk pallor is due to neural tissue thinning, not capillary loss, despite reduced capillary volume.

Quigley H A, Addicks E M

Scanning electron microscopy of glaucoma trabeculectomy specimens found no extracellular material obstructing inner meshwork pores, contradicting prior reports and suggesting different outflow resistance mechanisms.

Quigley H A, Flower R W, Addicks E M, McLeod D S

Studying acute IOP elevation in primate eyes, researchers found axonal transport blockade at the optic nerve head. Anoxia was not the main cause; mechanical compression likely drives this damage, challenging prior assumptions.

Quigley H A, Addicks E M

Primate eyes with elevated IOP showed axonal transport block at the lamina cribrosa. Even brief IOP elevation caused irreversible nerve damage and degeneration, highlighting glaucoma's rapid destructive potential.

Quigley H A, Addicks E M

This study confirmed that ghost red blood cells cause chronic elevated eye pressure in animals, mimicking secondary glaucoma. This provides a valuable model to study glaucoma's effects on ocular tissues.