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Pathogenesis of NTG seems to involve both IOP dependent and IOP independent mechanisms that work individually or in combination. Increased IOP can distort the lamina cribrosa and interfere with axoplasmatic flow or create hypo-perfusion of the optic nerve head. On the other hand a high incidence of vascular insufficiency has been demonstrated in NTG patients, leading to perfusion deficits of the optic nerve head, the retina, the choroid and the retro-bulbar vessels [2, 4-6]. For many years it was unclear whether lowering IOP in NTG patients from somewhere within the normal range to a lower value was useful. The Collaborative Normal Tension Glaucoma Study however showed that there was a slower progression of visual field loss in NTG patients with 30% or more lowering of their IOP [1].

Prospective Study on the Effect of Selective Laser Trabeculoplasty in Normal Tension Glaucoma