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Spontaneous venous pulsations should be monitored during glaucoma therapy
  1. C F Parsa
  1. Wilmer Ophthalmological Institute, Johns Hopkins University School of Medicine
  1. Correspondence to: Wilmer Ophthalmological Institute, Maumenee 517, 600 North Wolfe Street, Baltimore, MD 21287-9237, USA; cparsa{at}jhmi.edu

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It is well established that lowering intraocular pressure slows or halts progression of glaucoma. None the less, changes in intracranial pressure also affect the pressure gradient across the lamina cribrosa. Normal intraocular pressures combined with low intracranial pressures produce the same pressure differential across the laminae as elevated intraocular pressures in conjunction with normal intracranial pressures.1–3 Failing to factor in both intraocular and intracranial pressures may create an inappropriate distinction in the pathogenesis of glaucomas currently labelled as normal tension from those where elevated intraocular pressures can be recorded.1 Development of the optic neuropathy in glaucoma may be secondary to mechanical deformation and destruction of lamina cribrosa causing axonal degeneration, or conceivably to pressure related ischaemic events. A goal of therapy in either situation should be equalisation of prelaminar intraocular pressure with opposing retrolaminar tissue and cerebrospinal fluid pressure.

Spontaneous venous pulsations occur when intraocular pressure during systole exceeds central retinal venous pressure, which, in turn, reflects intracranial pressure transmitted through the perineural subarachnoid space and retrolaminar tissue pressure.2,4–6 Lowering intraocular pressure until venous pulsations cease minimises the pressure gradient between mean intraocular and retrolaminar pressure, and allows a clinical estimation of intracranial pressure. Keeping momentary fluctuations in mind, such end points may guide intraocular pressure lowering strategies to help avoid undertreatment or overtreatment of individuals with glaucoma. Therapies that lower intraocular pressure without also lowering intracranial pressure (such as topical rather than oral carbonic anhydrase inhibitors) should be favoured. The question of whether intracranial pressure raising strategies should be considered may arise in select cases. Finally, a consistent lack of spontaneous venous pulsations in patients with ocular hypertension, especially when venous pulsations can be elicited by digital pressure on the globe, may indicate sufficient counterbalancing intracranial pressure to render intraocular pressure reduction unnecessary.

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