AUG 06, 2013
The authors of this article propose an intriguing hypothesis on the pathogenesis of normal tension glaucoma (NTG) based on a literature review. They suggest that senescent changes in cerebrospinal fluid (CSF) circulatory physiology along with the translaminar pressure gradient can account for the pathophysiology of normal tension glaucoma.
They point out that CSF stasis could occur with aging and lead to neurotoxic byproducts not being cleared efficiently, which in turn could lead to glaucomatous damage. They suggest a link between diminished CSF production, circulation and outflow in Alzheimer disease and normal pressure hydrocephalus, and propose a similar mechanism for NTG.
However, they note that there is conflicting data regarding the incidence of glaucoma in the Alzheimer population. They also stress that their hypothesis of the pathogenesis of NTG remains unproven. They say that further research is necessary to determine the possible role of CSF circulatory dysfunction in NTG.