Abstract
Purpose:
Recent observations suggest that low levels of intracranial pressure (ICP) may be associated with the eventual development of glaucoma. The converse of that postulate seems worth exploring, that is, does elevated intracranial pressure protect against the eventual development of glaucomatous damage to the optic nerve? Idiopathic intracranial hypertension (IIH) is a clinical syndrome characterized by elevated ICP, disc edema, and an otherwise normal cerebrospinal fluid analysis. An exploration of such a population, and that population’s eventual risk of development of glaucoma, may afford a prism to explore the effects of elevated ICP upon the development of a pressure-related optic neuropathy.
Methods:
We compared the prevalence of primary open angle glaucoma (POAG) in IIH patients with that in an age-adjusted patient population served by Montefiore Medical Center to probe whether elevated ICP may afford some protection against the development of glaucoma. Two cohorts - one with IIH (N = 353) and the other comprised of Montefiore in-patients and out-patients (N = 646,698) - were assembled from a retrospective epidemiological review of our electronic medical record data set and its pool of more than 1.4 million patients and their encounters over the past 17 years.
Results:
The overall prevalence of POAG in the Montefiore patient population compared to the prevalence of POAG in the cohort that suffered from IIH was 1.84% vs. 0.28%. A Fisher's exact test was employed to compare the two groups’ prevalences; the difference between the two groups was found to be statistically significant with a p-value = 0.026.
Conclusions:
Intracranial pressure may be a clinically meaningful heretofore unrecognized factor in the development of glaucoma. Patients with IIH and elevated ICP may be less likely to develop primary open angle glaucoma; conversely, patients with low ICP may be at especial risk of glaucoma. Further investigation is necessary to evaluate whether our epidemiological observations that elevated ICP may modulate the development of POAG are valid.