It is well-known that IOP is a single, modifiable factor in determining the risk and further progression of glaucoma. As IOP is a measurement we use consistently in practice, it is worth learning about the roles the other pressures, namely, ocular perfusion pressure (OPP), cerebrospinal fluid pressure (CSFP) and blood pressure (BP), play in measuring IOP. (See “IOP: A Review,” p.20.)

Also featured in June:

Here’s a look at these pressures and the current action step associated with all of them.


In simple terms, OPP refers to the amount of blood flow delivered to ocular tissues. It is calculated as the difference between arterial BP and venous BP. Thus, OPP also can be thought of as the difference between arterial BP and IOP because IOP is similar to the value of venous BP. The exact formula to calculate OPP is: Mean OPP=2/3(diastolic BP+1/3(systolic BP/diastolic BP)-IOP.

A specific balance between arterial BP and venous BP is required to have adequate perfusion for any tissue. Ischemia results when tissues fed by blood vessels have poor perfusion. Therefore, an imbalance between arterial BP and venous BP can have devastating consequences on the optic nerve and, thus, has been linked to glaucomatous damage.1

The significance of OPP is that it has been linked with open-angle glaucoma in many population-based epidemiologic studies in the United States, Europe and Caribbean.

Specifically, a low diastolic perfusion pressure below 55 mmHg, was associated with open-angle glaucoma.2-5 The severity of normotensive, more recently called low-tension open-angle glaucoma, was strongly correlated with the circadian fluctuation of OPP.6 Also, the Early Manifest Glaucoma Trial indicates that a low systolic perfusion pressure at baseline reveals faster progression of glaucoma.7,8


CSFP is the true counter-pressure to IOP across the lamina cribrosa. Both the IOP and CSFP are important factors in determining the pliability of the optic nerve.1 Meaning, the IOP is the force pushing against the lamina cribrosa, and the CSFP pushes back. With a low CSFP or a high IOP, there is an imbalance in forces, which can result in deformation of the optic nerve head, known as cupping.

Imagine, for a moment, diving deep into the ocean. You can feel the atmospheric pressure increasing around you, as you go deeper. Your IOP is extremely high at significant depths, but because of your body’s autoregulation, your CSFP increases as well, maintaining the equilibrium and, therefore, this action does not cause an acute onset of glaucoma or permanent damage to the optic nerve. Thus, this balance always must be working to allow for proper nourishment of the optic nerve in a healthy, stress-free environment.2


BP is the pressure of the blood running through the circulatory system. It is affiliated with the heartbeat’s force and rate, as well as the arterial walls’ diameter and elasticity. Although the possible interactions of BP with IOP and glaucoma have been studied, the results are somewhat contradictory:

On the one hand, hypertension has been linked to a high IOP. Specifically, cross-sectional studies have suggested that each 10 mmHg higher systolic BP is related to 0.23 mmHg to 0.32 mmHg increase in IOP.2,4,11 These are similar to the values found in longitudinal studies, including the Beaver Dam and Barbados Eye Studies.12,13 That said, there has been no direct correlation to the onset of glaucomatous damage or progression.

On the other hand, low BP results in low OPP, which has been linked to inciting glaucomatous damage in addition to hastening progression rates of glaucoma. OPP is dependent on a complex process involving both IOP and BP, as explained above. Vascular dysregulation disrupts the equilibrium of arterial and venous pressures, which leads to ischemia. This has been proposed as a “vascular theory” for the underlying cause of glaucoma.14-16 As is the case with other diseases, such as diabetes, in which fluctuation in blood sugar is often more damaging than stable blood sugar, wide fluctuations in OPP also occur in situations of vascular dysregulation and seem to occur mostly at night when OPP is the lowest.

This is particularly relevant in normotensive glaucoma (NTG). In a study looking at nocturnal systemic hypotension and the risk of glaucoma progression, it was revealed that both the magnitude and duration of nocturnal hypotension is related to VF progression in patients who have NTG.17

The take home: Patients who show glaucoma progression, despite adequate and stable IOP decreases with reported compliance of their medications, specifically who have NTG, should be evaluated for nocturnal hypotension. Also, sleep apnea should be considered in such patients.18 In addition, it is worth having a conversation with the patient’s cardiologist or primary care doctor to determine whether aggressive hypertensive therapy is necessary and to recommend that these medications are not taken at bedtime.

IOP: A Review

IOP, broken down into “intra”-”ocular”-”pressure”, literally means the pressure inside the eye. But is that what we are measuring with our various tonometry techniques? IOP is defined as the pressure inside the anterior chamber with the addition of the atmospheric pressure. In effect, we are measuring the transcorneal pressure of the eye, which we then use as an indication of the translaminar pressure in our evaluations of risk. IOP is, therefore, one of two components of the translaminar pressure difference.


Glaucoma is an optic neuropathy that has long been associated with pressure. IOP is an indication of what the pressure might be across the optic nerve head and one of two components responsible for the translaminar pressure difference.

Although ocular hypertension is associated with the development and progression of glaucoma, it is not necessarily causative of glaucoma, and there is a large group of ocular hypertensive patients who never develop glaucoma.

Therefore, clearly, other factors are at play in determining glaucoma risk and disease progression. One important factor is OPP. Patients who have low or widely fluctuating OPP are at higher risk of glaucoma development as well as progression, particularly in the NTG patient subgroup.15


So, what can we do with the information provided above to help our glaucoma patients?

Unfortunately, no device is approved for measuring OPP at this time. Thus, the best we can do for our glaucoma patients presently is to measure BP and calculate OPP using the formula mentioned above.

In fact, as more is learned about OPP, optometrists should consider readying themselves to implement some form of regular BP monitoring of their patients in an office setting. This is particularly important for patients who have NTG and have shown disease progression or in patients who are known to be on aggressive hypertensive medications. OM

Special thanks to Michael Cymbor, O.D., F.A.A.O., for reviewing this article.


  1. Leske MC. Ocular perfusion pressure and glaucoma: clinical trial and epidemiologic findings. Curr Opin Ophthalmol. 2009; 20: 73-78.
  2. Tielsch JM, Katz J, Sommer A, Quigley HA, Javitt JC. Hypertension, perfusion pressure, and primary open-angle glaucoma. A population-based assessment. Arch Ophthalmol. 1995; 113: 216–21.
  3. Leske MC, Connell AM, Wu SY, Hyman LG, Schachat AP. Risk factors for open-angle glaucoma. The Barbados Eye Study. Arch Ophthalmol. 1995; 113: 918–24.
  4. Bonomi L, Marchini G, Marraffa M, Bernardi P, Morbio R, Varotto A. Vascular risk factors for primary open angle glaucoma: the Egna-Neumarkt Study. Ophthalmology. 2000; 107: 1287–93.
  5. Quigley HA, West SK, Rodriguez J, Munoz B, Klein R, Snyder R. The prevalence of glaucoma in a population-based study of Hispanic subjects: Proyecto VER. Arch Ophthalmol. 2001; 119: 1819–26.
  6. Choi J, Kim KH, Jeong J, Cho HS, Lee CH, Kook MS. Circadian fluctuation of mean ocular perfusion pressure is a consistent risk factor for normal-tension glaucoma. Invest Ophthalmol Vis Sci. 2007; 48: 104–11.
  7. Leske MC, Heijl A, Hyman L, et al. Predictors of long-term progression in the early manifest glaucoma trial. Ophthalmology. 2007; 114: 1965–172.
  8. Leske MC, Heijl A, Hyman L, Bengtsson B, Komaroff E. Factors for progression and glaucoma treatment: The Early Manifest Glaucoma Trial. Curr Opin Ophthalmol. 2004; 15: 102–6.
  9. Jonas JB, Wang N, Yang D, Ritch, R, Panda-Jonas S. Facts and myths of cerebrospinal fluid pressure for the physiology of the eye. Progress in Retinal and Eye Research. 2015; 46: 67-83.
  10. Ocular perfusion pressure, cerebrospinal fluid pressure: New players in glaucoma. Ophthalmology Times web site. . Published December 10, 2017. Accessed May 17, 218.
  11. Deokule S, Weinreb RN. Relationships among systemic blood pressure, intraocular pressure, and open-angle glaucoma. Can J Ophthalmol. 2008; 43: 302–7.
  12. Klein BE, Klein R, Knudtson MD. Intraocular pressure and systemic blood pressure: longitudinal perspective: the Beaver Dam Eye Study. Br J Ophthalmol. 2005; 89: 284–7.
  13. Wu SY, Leske MC. Associations with intraocular pressure in the Barbados Eye Study. Arch Ophthalmol. 1997; 115: 1572–6.
  14. Grieshaber MC, Mozaffarieh M, Flammer J. What is the link between vascular dysregulation and glaucoma? Surv Ophthalmol. 2007; 52(Suppl 2): S144–54.
  15. Nicolela MT. Clinical clues of vascular dysregulation and its association with glaucoma. Can J Ophthalmol. 2008; 43: 337–41.
  16. Flammer J, Mozaffarieh M. Autoregulation, a balancing act between supply and demand. Can J Ophthalmol. 2008; 43: 317–321.
  17. Charlson ME, De Moraes CG, Link A, et. al Nocturnal systemic hypotension increases the risk of glaucoma progression. Ophthalmology. 2014; 121: 2004-12.
  18. Biligan G. Normal Tension glaucoma and obstructive sleep apnea. BMC Ophthalmology. 2014; 14:27. doi: 10.1186/1471-2415-14-27.