[Mechanism study on trans-lamina cribrosa pressure difference correlated with optic neuropathy in glaucoma].

Glaucomatous optic neuropathy is among the most common causes of blindness worldwide. Elevated intraocular pressure (IOP) has long being considered to be the major risk factors for the development and progression of glaucomatous optic nerve damage. However, numerous studies have shown that a relatively large number of patients with typical glaucomatous optic neuropathy, in whom the IOP measurements have always been in the normal range (<21 mmHg, 1 mmHg = 0.133 kPa). Thus, the role of IOP in the pathogenesis of POAG becomes vague and controversial. Based on prospective clinical observations, Beijing iCOP (Intracranial and Intraocular Pressure) Study has found that the orbital cerebrospinal fluid pressure (CSF-P) may be of importance for the physiology and patho-physiology of the optic nerve head and may play a role in the pathogenesis of glaucomatous optic neuropathy. A low CSF-P in the retrobulbar region of the orbit may act as the counter-pressure against IOP and theoretically have a similar effect as an increased IOP on the trans-lamina cribrosa pressure difference which may be more relevant to the glaucomatous optic neuropathy than IOP alone. Moreover, an experimental and chronic reduction in CSF-P in monkeys was associated with the development of optic nerve damage morphologically typical for glaucomatous optic neuropathy. The findings support the hypothesis the CSF-P may play a role in the pathogenesis of glaucomatous optic neuropathy.