What causes elevated intraocular pressure (IOP) in primary open-angle glaucoma (POAG)?

Updated: Mar 16, 2020
  • Author: Kristin Schmid Biggerstaff, MD; Chief Editor: Inci Irak Dersu, MD, MPH  more...
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Answer

Other various theories (see Pathophysiology) have been advanced to explain the possible etiologic role of elevated IOP in glaucomatous optic neuropathy, as follows:

  • The mechanical compression theory suggests that elevated IOP causes a backward bowing of the lamina cribrosa, kinking the axons as they exit through the lamina pores. This may lead to focal ischemia, deprive the axons of neurotrophins, or interfere with axoplasmic flow, triggering cell death.

  • The vascular theories propose that cell death is triggered by ischemia, whether induced by elevated IOP or as a primary insult.

  • Other risk factors may play a role in the development of POAG, including a history of migraine headaches (a condition associated with vasospasm), cardiovascular disease, diabetes, systemic hypertension (leading to arteriosclerosis), and systemic hypotension (leading to decreased perfusion).

  • Genetic theories propose that cell death is triggered by genetic predisposition. Following the death of individual axons, substances may be released into the environment that causes a secondary triggering of apoptosis in neighboring cells, including glutamate (a neurotransmitter that may cause excitotoxicity), calcium, nitric oxide, and free radicals.


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