February 2005
Volume 46, Issue 2
Free
Glaucoma  |   February 2005
Relative Change in Diurnal Mean Ocular Perfusion Pressure: A Risk Factor for the Diagnosis of Primary Open-Angle Glaucoma
Author Affiliations
  • Mitra Sehi
    From the School of Optometry and the
  • John G. Flanagan
    From the School of Optometry and the
    Department of Ophthalmology and Vision Sciences, University of Toronto, Toronto, Canada.
  • Leilei Zeng
    Department of Statistics and Actuarial Science, University of Waterloo, Waterloo, Canada; and the
  • Richard J. Cook
    Department of Statistics and Actuarial Science, University of Waterloo, Waterloo, Canada; and the
  • Graham E. Trope
    Department of Ophthalmology and Vision Sciences, University of Toronto, Toronto, Canada.
Investigative Ophthalmology & Visual Science February 2005, Vol.46, 561-567. doi:10.1167/iovs.04-1033
  • Views
  • PDF
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Mitra Sehi, John G. Flanagan, Leilei Zeng, Richard J. Cook, Graham E. Trope; Relative Change in Diurnal Mean Ocular Perfusion Pressure: A Risk Factor for the Diagnosis of Primary Open-Angle Glaucoma. Invest. Ophthalmol. Vis. Sci. 2005;46(2):561-567. doi: 10.1167/iovs.04-1033.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

purpose. To investigate diurnal change and pattern of variation in intraocular pressure (IOP) and systolic (SBP) and diastolic (DSP) blood pressures in a group with untreated primary open-angle glaucoma (uPOAG) and compare it with an age-matched, normal group.

methods. IOP, SBP, and DBP were measured in 14 patients with uPOAG and in 14 normal subjects, every hour between 7 AM and 10 PM and the mean ocular perfusion pressure (MOPP) was calculated. Mixed-effect linear models were used to analyze the repeated-measures data in which both fixed and random effects were included. The relative diurnal change was calculated as the percentage decrease from maximum.

results. The uPOAG group had the higher IOP (P < 0.001) and lower MOPP (P = 0.025). There was a significant diurnal change in IOP, SBP, DBP, and MOPP in both groups (P < 0.001). The pattern of diurnal variation in IOP (P = 0.137), SBP (P = 0.569), and DBP (P = 0.937) was not significantly different between groups but was significantly different for MOPP (P = 0.040). MOPP and IOP were most similar at 7 AM and 1 PM. Postprandial hypotension was significant for SBP, DBP, and MOPP (P < 0.001), but not IOP (P = 0.388) in both groups. The relative change in MOPP was larger in the uPOAG group (38% vs. 26%, P < 0.001), but the change in IOP was similar (42% vs. 41%, P = 0.786). There was a significant effect of DBP on IOP over the course of the day in the uPOAG group (P = 0.011) but not in the normal group (P = 0.733).

conclusions. The relative diurnal change in IOP was similar in both uPOAG and normal subjects but MOPP showed a significant difference. MOPP significantly decreased after lunch, and was at its lowest in uPOAG at 7 AM, when IOP was at its highest. A significant association was found between diurnal DBP and IOP in uPOAG.

It has been proposed that vascular risk factors are among the major precipitating factors that lead to the development of glaucomatous optic neuropathy. 1 2 3 4 5 6 7 8 9 Blood flow in any tissue is generated by the perfusion pressure that is defined as the difference between mean arterial blood pressure (MAP) and venous pressure. In the resting position, MAP is calculated as 10 11  
\[\mathrm{MAP}\ {=}\ \mathrm{DBP}\ {+}\ \frac{1}{3}\mathrm{(SBP}\ {-}\ \mathrm{DBP)}\]
where the difference between the systolic (SBP) and diastolic (DBP) blood pressures is the pulse pressure. 11 In the eye, the venous pressure should be marginally higher than the intraocular pressure (IOP), to allow for adequate blood circulation. Therefore, for the calculation of the mean ocular perfusion pressure (MOPP), IOP is substituted for venous pressure 5 12 13 so that the MOPP in the the eye is equal to the difference between the MAP and IOP. 14 15 16  
\[\mathrm{MOPP}\ {=}\ \frac{2}{3}{[}\mathrm{DBP}\ {+}\ \frac{1}{3}\mathrm{(SBP}\ {-}\ \mathrm{DBP)}{]}\ {-}\ \mathrm{IOP}\]
The perfusion pressure changes during the day, but the tissue blood flow should remain stable, to maintain metabolic activity. 11 17 18 19 Diurnal variation of IOP has been well documented, 20 21 22 23 24 25 26 27 28 29 and it has been demonstrated that the range of IOP fluctuation is larger than normal in persons with untreated glaucoma (Heijl A, et al. IOVS 2004;45:ARVO E-Abstract 943). 20 23 24 25 27 29 30 31 32 Zeimer. 33 hypothesized that if the diurnal variation in IOP were a pure biorhythm, it could be described by a cosine function, in which the higher the IOP, the higher the amplitude and therefore the greater the diurnal change. 33 34 Recently, doubts have been raised about the idea that a large diurnal range of IOP is an independent risk factor for the development of glaucoma. Sacca et al. 32 studied diurnal fluctuations of IOP in three groups—primary open-angle glaucome (POAG), low-tension glaucoma, and normal—and found that the daily IOP fluctuations were directly proportional to the level of IOP. Heijl and Bengtsson (IOVS 2004;45:ARVO E-Abstract 943) demonstrated that in a group of patients who participated in a 10-year study of ocular hypertension, the higher the IOP, the larger the range of diurnal variation, and that diurnal variation in IOP was not an independent risk factor for development of glaucoma. However, mean IOP was found to be a strong risk factor. 
Diurnal variation of SBP has also been well studied (Sehi M, et al. IOVS 2004;45:ARVO E-Abstract 4447; Sehi M, et al. IOVS 2003;44:ARVO E-Abstract 979). 2 8 35 36 37 38 39 40 41 However, there are few studies regarding diurnal variation in MOPP 28 42 and its role as a risk factor for the diagnosis of POAG. 
The purpose of this study was to investigate the diurnal change and diurnal pattern of variation in IOP, SBP, and MOPP in a group of patients with newly diagnosed, early POAG, before treatment was begun, and to compare the results with those in a group of healthy, age-matched volunteers. 
Methods
This study was of a prospective cohort design. The sample consisted of two groups, patients with untreated (u)POAG and healthy, age-matched volunteers. Participants were recruited from clinics at the University of Waterloo and four private ophthalmology/optometry offices in the Waterloo region. Volunteers were excluded from the study if they had a history of systemic or ocular disease that would affect systemic or ocular blood flow, had taken medication that would affect the blood pressure or blood flow, had a central nervous system (CNS) disease, or had taken any prescribed medication for CNS disease within the previous 6 months or if they were smokers. 
Participants were eligible for entry into the uPOAG group if they were at least 35 years old, SBP was within the range of 90 to 139 mm Hg and resting DBP was <89 mm Hg, and IOP was >21 mm Hg and if they had received a diagnosis of POAG but had not started treatment. The diagnosis of POAG was made by a single glaucoma specialist (GET). 
Participants were eligible for entry into the normal group if SBP was within the range of 90 to 139 mm Hg and resting DBP was <89 mm Hg, IOP was <21 mm Hg, the glaucoma hemifield test (Humphrey Field Analyser 720; SITA-standard 30-2; Carl Zeiss Meditec, Dublin, CA) was within normal limits, and there was no sign of optic neuropathy. Normal volunteers were age matched to the uPOAG group. 
Ethics approval was granted by the Office of Research at the University of Waterloo. All procedures conformed to the Declaration of Helsinki. Informed consent was obtained from each volunteer after explanation of the nature and possible consequences of the study. All volunteers avoided activities that could increase the blood pressure or heart rate, such as climbing stairs. Meals were provided at 12:30 and 6:30 PM but did not include alcohol, tea, coffee, or additional salt. Volunteers drank one cup of tea or coffee between 9 and 10 AM. One investigator (MS) completed all measurements. Blood pressure was measured with a brachial mercurial sphygmomanometer on the left arm after the subject had been seated for at least 3 minutes. The IOP and SBP were measured every hour between 7 AM and 10 PM during a single 1-day session. The assessment of IOP was performed with a slit-lamp–mounted Goldmann applanation tonometer. Central corneal thickness (CCT) was measured once in the midmorning with an ultrasound pachymeter (DGH-550 Pachette 2; DGH Technology, Inc., Exton, PA). 43 IOP was adjusted 3 mmHg for every 50 μm that the corneal thickness deviated from an average of 535 μm. 44 The ocular perfusion pressure was calculated as the difference between two thirds of the MAP and IOP. 15 In the glaucoma group, the eye with stronger evidence of glaucoma was selected for participation in the study. In the normal group, the test eye was selected randomly. 
Analysis for repeated-measures data was conducted to characterize diurnal variation by using mixed-effect linear models that include both fixed and random effects. Coefficients of explanatory variables were treated as fixed effects, as in standard linear models, and the intercept was treated as a random effect, to accommodate correlations in the responses within patients over assessments. The explanatory variables considered included time, an indicator of whether a participant was normal or a patient with uPOAG (disease variable), and the associated interactions (time and disease). The explanatory variables were selected to provide insight into patterns of diurnal variation in ocular perfusion pressures in both normal and patients with uPOAG. 45  
Absolute and relative diurnal changes for each outcome measure were calculated. The absolute diurnal change—the difference between maximum and minimum values (range)—was determined for each individual, and the average was calculated for each group. The relative diurnal change—the percentage decrease from maximum (or range divided by maximum)—was determined for each individual, and the average was calculated for each group. The between-group comparisons were analyzed using unpaired two-tailed Student’s t-test. 
The association between SBP and IOP was also examined by using mixed-effect linear models. IOP was considered to be the response of interest, and the explanatory variables included patient group, time, SBP, and DBP and the interaction between the last three variables and patient group. 
Results
Fourteen volunteers with uPOAG (mean age, 56.3 ± 12 years; 7 women) and 14 healthy age-matched volunteers (mean age, 57.6 ± 9.9 years; 9 women) were examined. All 28 volunteers were white. 
There was a significant diurnal change in IOP in both the uPOAG and normal groups compared to the 7 AM baseline (P < 0.001; Fig. 1 ). The mean IOP was significantly higher in patients with uPOAG than in normal subjects throughout the day (19.2 and 13.0 mm Hg, respectively; P < 0.001; Table 1 ). The absolute diurnal change was greater in the uPOAG group (10.3 ± 2 mm Hg, uPOAG; and 6.4 ± 1.4 mm Hg, normal; P < 0.001). The maximum IOP for both groups was recorded at 7 AM (9/14 uPOAG, 8/14 normal subjects), with the uPOAG group mean IOP being significantly higher (by 7.9 mm Hg; P < 0.001). The pattern of diurnal variation in IOP relative to the 7 AM value was not significantly different between patients with uPOAG and normal subjects (time and disease interaction; P = 0.137). In summary, there was a significant diurnal change in IOP in both groups, but the pattern of diurnal variation was similar in both groups. 
There was a significant diurnal change in SBP in both the uPOAG and normal groups compared with the level at 7 AM (P < 0.001; Fig. 2 ). The mean SBP was not significantly different between the two groups (Table 1 ; P = 0.543) throughout the day. There was a significant increase in SBP from 4 PM when compared with that at 7 AM, for both groups; however, the pattern of diurnal variation was not significantly different between groups (time and disease interaction; P = 0.233). 
There was a significant diurnal change in DBP in both the uPOAG and normal groups compared with the 7 AM reading (P < 0.001; Fig. 3 ). The mean DBP was not significantly different between the two groups (Table 1 ; P = 0.954) throughout the day. The pattern of diurnal variation was comparable for uPOAG and normal groups (time and disease interaction; P = 0.550). 
There was a significant diurnal change in MOPP in both the uPOAG and normal groups compared with that at 7 AM (P < 0.001; Fig. 4 ). The mean MOPP was significantly lower in patients with uPOAG than in normal subjects (42.0 and 47.6 mm Hg, respectively; P = 0.024; Table 1 ) throughout the day, and the absolute diurnal change was greater in the uPOAG group (19.2 ± 3.8 mm Hg uPOAG; 14.4 ± 3.2 mm Hg normal; P = 0.001). The minimum MOPP in the uPOAG group was recorded at 7 AM (mean 35.5 mm Hg), and it was significantly lower than normal subjects at this time (8.8 mm Hg; P = 0.003). The pattern of diurnal variation in MOPP relative to the 7 AM level was significantly different between patients with uPOAG and normal subjects (time and disease interaction; P = 0.040). Specifically, the MOPP was elevated at 2 PM and at the end of the day (from 8 PM) in the uPOAG group, but in the normal group there was only a slight increase. In summary, there was a significant diurnal change in MOPP in both groups, and the pattern of diurnal variation was different between groups. 
There was significant postprandial hypotension in SBP (P < 0.003) and DBP (P < 0.001). We also found a significant postprandial hypotension in MOPP (P < 0.001) in both groups. IOP showed no significant change in either group after lunch (P = 0.642 uPOAG; P = 0.069 normal). 
The percentage decrease (relative change) in IOP was similar between patients with uPOAG and normal subjects (42% and 41%, respectively; P = 0.786). We did not find any significant difference between the percentage decrease in SBP (20% and 19.6%, respectively, P = 0.878) or DBP (24%, 21%, P = 0.263) in either group. When we compared the percentage decrease in MOPP, we found a significant difference between uPOAG and normal subjects (38% and 26%, respectively, P < 0.001). There was no correlation between the change in SBP and the change in IOP for the uPOAG group, during the course of the day (P = 0.736). However, the change in DBP had a significant effect on IOP (P = 0.011) such that for every 1 mm Hg increase in DBP, the IOP increased 0.086 mm Hg. In the normal group, neither SBP (P = 0.585) nor DBP (P = 0.733) had a significant effect on IOP over the course of the day. 
Discussion
In patients with untreated glaucoma, the diurnal change in IOP has been reported to be between 4.8 and 18.4 mm Hg, 46 47 whereas, in the normal eyes, it has been reported to be between 2.8 and 6.5 mm Hg. 48 49 Our uPOAG group fell within this range, with an average diurnal change in IOP of 10.3 ± 2.8 mm Hg after correcting for corneal thickness (9.75 ± 2.8 mm Hg before correcting for corneal thickness). However, our normal group had an average diurnal change in IOP of 6.8 ± 1.4 mm Hg, slightly higher than previously reported normal IOP, after correcting for corneal thickness (6.75 ± 1.5 mm Hg before correcting for CCT). Interstudy comparisons are difficult, because study designs are frequently different—for example, in terms of gender distribution, 50 51 age group, 50 race, 52 53 type of tonometer, 20 49 54 55 56 57 58 59 60 frequency of measurement and starting time, 21 27 61 62 63 corneal thickness considerations, 52 64 65 66 67 68 69 and the calculation of the diurnal change (Heijl A, et al. IOVS 2004;45:ARVO E-Abstract 943). 20 26 27 29 42 48 54 55 60 62 63 71 72 73 74 In many of these studies, the diurnal change was calculated by using the maximum and minimum of the group mean IOP at each measurement time, rather than the average of the individual diurnal changes in IOP that we used. Our method of calculating diurnal change was consistent with that used by Heijl and Bengtsson (IOVS 2004;45:ARVO E-Abstract 943). However, if we calculate the diurnal change using the alternate method, our results would be 6.5 mm Hg for the uPOAG group and 4.1 mm Hg for the normal group, well within the previously reported ranges. 
Postprandial systemic hypotension is a well-known phenomenon. 39 40 41 75 The impact of postprandial reduction of cerebral perfusion has also been reported. 75 76 77 78 However, to the best of our knowledge, this is the first report of postprandial reduction in ocular perfusion pressure in both patients with uPOAG and normal volunteers. It is uncertain why the decline of MOPP was not significant after the evening meal. We did not study the association between the level of MOPP decrease and the meal size, but an association has been reported in the past between blood pressure and meal size. 79 80 81  
It has been reported that as IOP increases, the eye maintains perfusion until the IOP is 6 mm Hg below the ocular perfusion pressure. 16 82 83 84 Figure 5shows the diurnal profile of IOP and MOPP in a patient with an asymmetric presentation of glaucoma. In the right eye, the eye with the most obvious glaucoma, there were periods of marked ocular perfusion decline early in the morning and after lunch, during which time, the optic nerve would be prone to ischemia. 
It has been suggested that large diurnal variation in IOP is an independent risk factor for the development of glaucoma. 20 24 29 70 85 In our study, although the absolute diurnal change in IOP was different between patients with uPOAG and normal subjects, we found that the relative diurnal change in IOP, expressed as a percentage of the maximum level, was similar between uPOAG and age-matched normal subjects. These results agree with Zeimer’s hypothesis 33 and the studies of Heijl and Bengtsson (IOVS 2004;45:ARVO E-Abstract 943) and Sacca et al., 32 who found that the daily IOP fluctuations were directly proportional to IOP level. They suggested that diurnal variation in IOP was therefore not an independent risk factor for development of glaucoma. Our results agree with these previous studies and also suggest that diurnal IOP should not be considered a risk factor for the diagnosis of POAG. 
We found that the percentage decrease in MOPP was significantly different between uPOAG and age-matched normal subjects. The mixed-effect linear model supported these findings, as the pattern of diurnal variation in MOPP was significantly different between patients with uPOAG and normal subjects. The difference between groups is somewhat exaggerated in the MOPP diurnal curve, due to the cumulative effect of a higher IOP and lower BP. This was particularly noticeable at 7 AM in the uPOAG group. 
Our findings suggest that the absolute diurnal measures of IOP alone are of limited clinical value in the diagnosis of POAG, but should be considered in conjunction with measures of diurnal systemic BP. We propose that the relative diurnal change in MOPP be considered a risk factor for the diagnosis of POAG. Our results also revive the debate with respect to the impact of treatment for systemic hypertension in patients with glaucoma—that is, a reduction in DBP of 12.5 mm Hg or in SBP of 25 mm Hg has the same impact on MOPP as an increase in IOP of 5 mm Hg. 
A positive correlation between SBP and IOP has been reported in patients with glaucoma. 1 2 61 67 86 87 88 89 90 91 We found no difference between the uPOAG and normal groups in the level of SBP and DBP, but there was a significant association between diurnal variation in DBP and IOP in patients with uPOAG, such that a 1-mm Hg increase in DBP was associated with a 0.09 mm Hg increase in IOP. It is important to clarify that our results do not suggest a simple relationship between hypertension and IOP, as all our participants had normal blood pressure. Our results indicate that there was a significant effect of DBP on IOP over the course of the day in patients with uPOAG that was not apparent in normal subjects. This does not imply that the association is causative, as it is most likely an indication of vascular dysfunction in the uPOAG group. 
In conclusion, the relative change in diurnal MOPP distinguished patients with uPOAG from normal subjects, but the relative change in IOP was did not. The assessment of MOPP may be a useful clinical tool for the diagnosis of early glaucoma. Change in DBP had a significant effect on IOP over the course of the day. There was postprandial hypotension in MOPP in both groups, which should be considered when evaluating ocular perfusion. MOPP was at its lowest in uPOAG at 7 AM when IOP was at its highest. The effect of periods of reduced ocular perfusion pressure on optic nerve head blood flow remains to be answered. Such studies are ongoing in our laboratory. 
 
Figure 1.
 
Group mean diurnal variation of IOP ± SE.
Figure 1.
 
Group mean diurnal variation of IOP ± SE.
Table 1.
 
Diurnal Pressures
Table 1.
 
Diurnal Pressures
IOP SBP DBP MOPP MOPP-IOP
POAG 19.2 ± 5.0 128.6 ± 11.3 73.6 ± 8.4 42.0 ± 7.1 22.7 ± 11.0
NORMALS 13.0 ± 3.0 125.9 ± 13.6 73.4 ± 6.9 47.6 ± 6.1 34.7 ± 7.9
Figure 2.
 
Group mean diurnal variation of SBP ± SE.
Figure 2.
 
Group mean diurnal variation of SBP ± SE.
Figure 3.
 
Group mean diurnal variation of DBP ± SE.
Figure 3.
 
Group mean diurnal variation of DBP ± SE.
Figure 4.
 
Group mean diurnal variation of MOPP ± SE.
Figure 4.
 
Group mean diurnal variation of MOPP ± SE.
Figure 5.
 
Diurnal IOP and MOPP in a patient with an asymmetric presentation of glaucoma. The difference between perfusion pressure and IOP was much less in the right eye, which had the more advanced signs of glaucoma.
Figure 5.
 
Diurnal IOP and MOPP in a patient with an asymmetric presentation of glaucoma. The difference between perfusion pressure and IOP was much less in the right eye, which had the more advanced signs of glaucoma.
Table 2.
 
The Absolute and Percentage Diurnal Changes in IOP and MOPP
Table 2.
 
The Absolute and Percentage Diurnal Changes in IOP and MOPP
IOP Change (Absolute) IOP Change (Relative, %) MOPP Change (Absolute) MOPP Change (Relative, %)
uPOAG 10.3 ± 2.8 42 ± 11 19.2 ± 3.8 38 ± 7
Normals 6.8 ± 1.4 41 ± 7 14.4 ± 3.2 26 ± 5
BonomiL, MarchiniG, MarraffaM, BernardiP, MorbioR, VarottoA. Vascular risk factors for primary open angle glaucoma: the Egna-Neumarkt Study. Ophthalmology. 2000;107:1287–1293. [CrossRef] [PubMed]
Bresson-DumontH, BechetoilleA. Role of arterial blood pressure in the development of glaucomatous lesions (in French). J Fr Ophtalmol. 1996;19:435–442. [PubMed]
CioffiGA, SullivanP. The effect of chronic ischemia on the primate optic nerve. Eur J Ophthalmol. 1999;9(suppl 1)S34–S36. [PubMed]
CostaVP, HarrisA, StefanssonE, et al. The effects of antiglaucoma and systemic medications on ocular blood flow. Prog Retin Eye Res. 2003;22:769–805. [CrossRef] [PubMed]
FlammerJ, OrgulS. Optic nerve blood-flow abnormalities in glaucoma. Prog Retin Eye Res. 1998;17:267–289. [CrossRef] [PubMed]
FlammerJ, OrgulS, CostaVP, et al. The impact of ocular blood flow in glaucoma. Prog Retin Eye Res. 2002;21:359–393. [CrossRef] [PubMed]
Fuchsjager-MayrlG, WallyB, GeorgopoulosM, et al. Ocular blood flow and systemic blood pressure in patients with primary open-angle glaucoma and ocular hypertension. Invest Ophthalmol Vis Sci. 2004;45:834–839. [CrossRef] [PubMed]
HayrehSS, ZimmermanMB, PodhajskyP, AlwardWL. Nocturnal arterial hypotension and its role in optic nerve head and ocular ischemic disorders. Am J Ophthalmol. 1994;117:603–624. [CrossRef] [PubMed]
KataiN, YoshimuraN. Apoptotic retinal neuronal death by ischemia-reperfusion is executed by two distinct caspase family proteases. Invest Ophthalmol Vis Sci. 1999;40:2697–2705. [PubMed]
AndersonDR. Introductory comments on blood flow autoregulation in the optic nerve head and vascular risk factors in glaucoma. Surv Ophthalmol. 2004;43:S5–S9.
SherwoodL. Human Physiology: from Cells to Systems. 2004; 5th ed.Brooks Cole Pacific Grove, CA.
AndersonDR. Introductory comments on blood flow autoregulation in the optic nerve head and vascular risk factors in glaucoma. Surv Ophthalmol. 2004;43:S5–S9.
HayrehSS. Blood flow in the optic nerve head and factors that may influence it. Prog Retin Eye Res. 2001;20:595–624. [CrossRef] [PubMed]
HayrehSS. The blood supply of the optic nerve head and the evaluation of it: myth and reality. Prog Retin Eye Res. 2001;20:563–593. [CrossRef] [PubMed]
GherghelD, OrgulS, GugletaK, GekkievaM, FlammerJ. Relationship between ocular perfusion pressure and retrobulbar blood flow in patients with glaucoma with progressive damage. Am J Ophthalmol. 2000;130:597–605. [CrossRef] [PubMed]
BisantisC. Ocular blood flow and its autoregulation.BucciMG eds. Glaucoma: Decision Making in Therapy. 1996;37–40.Springer-Verlag Milan.
AndersonDR. Introductory comments on blood flow autoregulation in the optic nerve head and vascular risk factors in glaucoma. Surv Ophthalmol. 2004;43:S5–S9.
PillunatLE, AndersonDR, KnightonRW, JoosKM, FeuerWJ. Autoregulation of human optic nerve head circulation in response to increased intraocular pressure. Exp Eye Res. 1997;64:737–744. [CrossRef] [PubMed]
RivaCE, HeroM, TitzeP, PetrigB. Autoregulation of human optic nerve head blood flow in response to acute changes in ocular perfusion pressure. Graefes Arch Clin Exp Ophthalmol. 1997;235:618–626. [CrossRef] [PubMed]
AsraniS, ZeimerR, WilenskyJ, GieserD, VitaleS, LindenmuthK. Large diurnal fluctuations in intraocular pressure are an independent risk factor in patients with glaucoma. J Glaucoma. 2000;9:134–142. [CrossRef] [PubMed]
DranceSM. Diurnal variation of intraocular pressure in treated glaucoma. Significance in patients with chronic simple glaucoma. Arch Ophthalmol. 1963;70:302–311. [CrossRef] [PubMed]
DranceSM. The value of diurnal tension studies in the early diagnosis and management of treatment in chronic simple glaucoma. Trans Can Ophthalmol Soc. 1963;26:210–224.
FontanaL, ArmasR, Garway-HeathDF, BunceCV, PoinoosawmyD, HitchingsRA. Clinical factors influencing the visual prognosis of the fellow eyes of normal tension glaucoma patients with unilateral field loss. Br J Ophthalmol. 1999;83:1002–1005. [CrossRef] [PubMed]
HughesE, SpryP, DiamondJ. 24-hour monitoring of intraocular pressure in glaucoma management: a retrospective review. J Glaucoma. 2003;12:232–236. [CrossRef] [PubMed]
IshikawaK, TaninoT, OhtakeY, KimuraI, MiyataH, MashimaY. A comparison of visual field and optic disc appearance depending on the peak intraocular pressure in patients with normal-tension glaucoma (in Japanese). Nippon Ganka Gakkai Zasshi. 2003;107:433–439. [PubMed]
LiuJH. Diurnal measurement of intraocular pressure. J Glaucoma. 2001;10:S39–S41. [CrossRef] [PubMed]
LiuJH, ZhangX, KripkeDF, WeinrebRN. Twenty-four-hour intraocular pressure pattern associated with early glaucomatous changes. Invest Ophthalmol Vis Sci. 2003;44:1586–1590. [CrossRef] [PubMed]
LiuJH, GokhalePA, LovingRT, KripkeDF, WeinrebRN. Laboratory assessment of diurnal and nocturnal ocular perfusion pressures in humans. J Ocul Pharmacol Ther. 2003;19:291–297. [CrossRef] [PubMed]
WilenskyJT. The role of diurnal pressure measurements in the management of open angle glaucoma. Curr Opin Ophthalmol. 2004;15:90–92. [CrossRef] [PubMed]
MishimaHK, KiuchiY, TakamatsuM, RaczP, BitoLZ. Circadianintraocular pressure management with latanoprost: diurnal and nocturnal intraocular pressure reduction and increased uveoscleral outflow. Surv Ophthalmol. 1997;41(suppl 2)S139–S144. [CrossRef] [PubMed]
HeijlA, LeskeMC, BengtssonB, HymanL, BengtssonB, HusseinM. Reduction of intraocular pressure and glaucoma progression: results from the Early Manifest Glaucoma Trial. Arch Ophthalmol. 2002;120:1268–1279. [CrossRef] [PubMed]
SaccaSC, RolandoM, MarlettaA, MacriA, CerquetiP, CiurloG. Fluctuations of intraocular pressure during the day in open-angle glaucoma, normal-tension glaucoma and normal subjects. Ophthalmologica. 1998;212:115–119.
ZeimerR.RitchR ShieldsMB KrupinT eds. The Glaucomas. 1996; 2nd ed. 429–445.Mosby St Louis.
NelsonW, TongYL, LeeJK, HalbergF. Methods for cosinor-rhythmometry. Chronobiologia. 1979;6:305–323. [PubMed]
BeilinLJ. Role of automated measurements in understanding lifestyle effects on blood pressure. Blood Press Monit. 2002;7:45–50. [CrossRef] [PubMed]
ClaridgeKG, SmithSE. Diurnal variation in pulsatile ocular blood flow in normal and glaucomatous eyes. Surv Ophthalmol. 1994;38(suppl)S198–S205. [CrossRef] [PubMed]
CollignonN, DeweW, GuillaumeS, Collignon-BrachJ. Ambulatory blood pressure monitoring in glaucoma patients: the nocturnal systolic dip and its relationship with disease progression. Int Ophthalmol. 1998;22:19–25. [CrossRef] [PubMed]
HayrehSS, PodhajskyP, ZimmermanMB. Beta-blocker eyedrops and nocturnal arterial hypotension. Am J Ophthalmol. 1999;128:301–309. [CrossRef] [PubMed]
KoharaK, UemuraK, TakataY, OkuraT, KitamiY, HiwadaK. Postprandial hypotension: evaluation by ambulatory blood pressure monitoring. Am J Hypertens. 1998;11:1358–1363. [CrossRef] [PubMed]
KruszewskiP, BieniszewskiL, Neubauer-GerykJ, SwierblewskaE, Krupa-WojciechowskaB. Supine body position is an important factor influencing postprandial ambulatory blood pressure. Med Sci Monit. 2003;9:CR34–CR41. [PubMed]
SchulzeMB, KrokeA, SaracciR, BoeingH. The effect of differences in measurement procedure on the comparability of blood pressure estimates in multi-centre studies. Blood Press Monit. 2002;7:95–104. [CrossRef] [PubMed]
LiuCJ, KoYC, ChengCY, et al. Changes in intraocular pressure and ocular perfusion pressure after latanoprost 0.005% or brimonidine tartrate 0.2% in normal-tension glaucoma patients. Ophthalmology. 2002;109:2241–2247. [CrossRef] [PubMed]
GordonMO, BeiserJA, BrandtJD, et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120:714–720. [CrossRef] [PubMed]
DoughtyMJ, ZamanML. Human corneal thickness and its impact on intraocular pressure measures: a review and meta-analysis approach. Surv Ophthalmol. 2000;44:367–408. [CrossRef] [PubMed]
McCullochCE, SearleSR. Generalized, Linear, and Mixed Models. 2001;John Wiley & Sons Toronto.
YamagamiJ, AraieM, AiharaM, YamamotoS. Diurnal variation in intraocular pressure of normal-tension glaucoma eyes. Ophthalmology. 1993;100:643–650. [CrossRef] [PubMed]
WorthenDM. Effect of pilocarpine drops on the diurnal intraocular pressure variation in patients with glaucoma. Invest Ophthalmol. 1976;15:784–787. [PubMed]
HornovaJ. Normal intraocular pressure values in the Czech population (in Czech). Cesk Slov Oftalmol. 1997;53:88–93. [PubMed]
KitazawaY, HorieT. Diurnal variation of intraocular pressure in primary open-angle glaucoma. Am J Ophthalmol. 1975;79:557–566. [CrossRef] [PubMed]
QureshiIA. Intraocular pressure: a comparative analysis in two sexes. Clin Physiol. 1997;17:247–255. [CrossRef] [PubMed]
PointerJS. Evidence that a gender difference in intraocular pressure is present from childhood. Ophthalmic Physiol Opt. 2000;20:131–136. [CrossRef] [PubMed]
ShimmyoM, RossAJ, MoyA, MostafaviR. Intraocular pressure, Goldmann applanation tension, corneal thickness, and corneal curvature in Caucasians, Asians, Hispanics, and African Americans. Am J Ophthalmol. 2003;136:603–613. [CrossRef] [PubMed]
MillerE. Race and the risk of glaucoma. Arch Ophthalmol. 2004;122:909–910. [CrossRef] [PubMed]
DavidR, ZangwillL, BriscoeD, DaganM, YagevR, YassurY. Diurnal intraocular pressure variations: an analysis of 690 diurnal curves. Br J Ophthalmol. 1992;76:280–283. [CrossRef] [PubMed]
DranceSM. The significance of the diurnal phasic variation of intraocular pressure in normal and glaucomatous eyes. Trans Can Ophthalmol Soc. 1960;23:131–140.
DranceSM. The significance of the diurnal tension variations in normal and glaucomatous eyes. Arch Ophthalmol. 1960;64:494–501. [CrossRef] [PubMed]
LagerlofO. Airpuff tonometry versus applanation tonometry. Acta Ophthalmol (Copenh). 1990;68:221–224. [PubMed]
PlagwitzKU, LemkeK. New measuring method of non-contact tonometry (in Germany). Klin Monatsbl Augenheilkd. 1999;214:40–43. [CrossRef] [PubMed]
Sarrion FerreMT, HervasJM, Blanquer GregoriJJ, Mulet PonsMJ, MarinRN, BareaMA. Screening for glaucoma in diabetic patients by using the Schiortz tonometer (in Spanish). Aten Primaria. 1996;17:18–22. [PubMed]
WilenskyJT, GieserDK, DietscheML, MoriMT, ZeimerR. Individual variability in the diurnal intraocular pressure curve. Ophthalmology. 1993;100:940–944. [CrossRef] [PubMed]
BengtssonB. Some factors affecting the distribution of intraocular pressures in a population. Acta Ophthalmol (Copenh). 1972;50:33–46. [PubMed]
XiXR, QureshiIA, WuXD, HuangYB, LuH, ShiarkarE. Diurnal variation of intraocular pressure in normal and ocular hypertensive subjects of China. J Pak Med Assoc. 1996;46:171–174. [PubMed]
BuguetA, PyP, RomanetJP. 24-hour (nyctohemeral) and sleep-related variations of intraocular pressure in healthy white individuals. Am J Ophthalmol. 1994;117:342–347. [CrossRef] [PubMed]
AakreBM, DoughtyMJ, DalaneOV, BergA, AamodtO, GangstadH. Assessment of reproducibility of measures of intraocular pressure and central corneal thickness in young white adults over a 16-h time period. Ophthalmic Physiol Opt. 2003;23:271–283. [CrossRef] [PubMed]
DaveH, KutschanA, PauerA, WiegandW. Measurement of corneal thickness in glaucoma patients [in German]. Ophthalmologe. 2004;101:919–924. [PubMed]
FosterPJ, BaasanhuJ, AlsbirkPH, MunkhbayarD, UranchimegD, JohnsonGJ. Central corneal thickness and intraocular pressure in a Mongolian population. Ophthalmology. 1998;105:969–973. [CrossRef] [PubMed]
FosterPJ, MachinD, WongTY, et al. Determinants of intraocular pressure and its association with glaucomatous optic neuropathy in Chinese Singaporeans: the Tanjong Pagar Study. Invest Ophthalmol Vis Sci. 2003;44:3885–3891. [CrossRef] [PubMed]
NomuraH, AndoF, NiinoN, ShimokataH, MiyakeY. The relationship between intraocular pressure and refractive error adjusting for age and central corneal thickness. Ophthalmic Physiol Opt. 2004;24:41–45. [CrossRef] [PubMed]
ShahS, SpeddingC, BhojwaniR, KwartzJ, HensonD, McLeodD. Assessment of the diurnal variation in central corneal thickness and intraocular pressure for patients with suspected glaucoma. Ophthalmology. 2000;107:1191–1193. [CrossRef] [PubMed]
ThomasR, ParikhR, GeorgeR, KumarRS, MuliyilJ. Five-year risk of progression of ocular hypertension to primary open angle glaucoma: a population-based study. Indian J Ophthalmol. 2003;51:329–333. [PubMed]
KitazawaY. Open-angle glaucoma clinical presentation and management (in Japanese). Nippon Ganka Gakkai Zasshi. 2001;105:828–842. [PubMed]
KatavistoM. The diurnal variations of ocular tension in glaucoma. Acta Ophthalmol (Copenh). 1964;46(suppl 78)1–130.
De VeneciaG, DavisM. Diurnal variation of intraocular pressure in the normal eye. Arch Ophthalmol. 1963;69:752–757. [CrossRef] [PubMed]
LiuJH, KripkeDF, TwaMD, et al. Twenty-four-hour pattern of intraocular pressure in the aging population. Invest Ophthalmol Vis Sci. 1999;40:2912–2917. [PubMed]
RakicV, BeilinLJ, BurkeV. Effect of coffee and tea drinking on postprandial hypotension in older men and women. Clin Exp Pharmacol Physiol. 1996;23:559–563. [CrossRef] [PubMed]
HilzMJ, MartholH, NeundorferB. Syncope: a systematic overview of classification, pathogenesis, diagnosis and management (in German). Fortschr Neurol Psychiatr. 2002;70:95–107. [CrossRef] [PubMed]
KrajewskiA, FreemanR, RuthazerR, KelleyM, LipsitzLA. Transcranial Doppler assessment of the cerebral circulation during postprandial hypotension in the elderly. Jam Geriatr Soc. 1993;41:19–24. [CrossRef]
LipsitzLA. Abnormalities in blood pressure homeostasis that contribute to falls in the elderly. Clin Geriatr Med. 1985;1:637–648. [PubMed]
Puvi-RajasinghamS, MathiasCJ. Effect of meal size on post-prandial blood pressure and on postural hypotension in primary autonomic failure. Clin Auton Res. 1996;6:111–114. [CrossRef] [PubMed]
SideryMB, MacdonaldIA. The effect of meal size on the cardiovascular responses to food ingestion. Br J Nutr. 1994;71:835–848. [CrossRef] [PubMed]
FaganTC, SawyerPR, GourleyLA, LeeJT, GaffneyTE. Postprandial alterations in hemodynamics and blood pressure in normal subjects. Am J Cardiol. 1986;58:636–641. [CrossRef] [PubMed]
WeiterJJ, SchacharRA, ErnestJT. Control of intraocular blood flow. II. Effects of sympathetic tone. Invest Ophthalmol. 1973;12:332–334. [PubMed]
RivaCE, GrunwaldJE, PetrigBL. Reactivity of the human retinal circulation to darkness: a laser Doppler velocimetry study. Invest Ophthalmol Vis Sci. 1983;24:737–740. [PubMed]
BestM, BlumenthalM, FuttermanHA, GalinMA. Critical closure of intraocular blood vessels. Arch Ophthalmol. 1969;82:385–392. [CrossRef] [PubMed]
BrubakerRF. Targeting outflow facility in glaucoma management. Surv Ophthalmol. 2003;48(suppl 1)S17–S20. [CrossRef] [PubMed]
DielemansI, VingerlingJR, AlgraD, HofmanA, GrobbeeDE, de JongPT. Primary open-angle glaucoma, intraocular pressure, and systemic blood pressure in the general elderly population. The Rotterdam Study. Ophthalmology. 1995;102:54–60. [CrossRef] [PubMed]
KleinBE, KleinR, LintonKL. Intraocular pressure in an American community. The Beaver Dam Eye Study. Invest Ophthalmol Vis Sci. 1992;33:2224–2228. [PubMed]
FlammerJ. The vascular concept of glaucoma. Surv Ophthalmol. 1994;38(suppl)S3–S6. [CrossRef] [PubMed]
GanleyJP. Epidemiological aspects of ocular hypertension. Surv Ophthalmol. 1980;25:130–135. [CrossRef] [PubMed]
LeskeMC, Warheit-RobertsL, WuSY. Open-angle glaucoma and ocular hypertension: the Long Island Glaucoma Case-Control Study. Ophthalmic Epidemiol. 1996;3:85–96. [CrossRef] [PubMed]
MitchellP, LeeAJ, RochtchinaE, WangJJ. Open-angle glaucoma and systemic hypertension: the blue mountains eye study. J Glaucoma. 2004;13:319–326. [CrossRef] [PubMed]
Figure 1.
 
Group mean diurnal variation of IOP ± SE.
Figure 1.
 
Group mean diurnal variation of IOP ± SE.
Figure 2.
 
Group mean diurnal variation of SBP ± SE.
Figure 2.
 
Group mean diurnal variation of SBP ± SE.
Figure 3.
 
Group mean diurnal variation of DBP ± SE.
Figure 3.
 
Group mean diurnal variation of DBP ± SE.
Figure 4.
 
Group mean diurnal variation of MOPP ± SE.
Figure 4.
 
Group mean diurnal variation of MOPP ± SE.
Figure 5.
 
Diurnal IOP and MOPP in a patient with an asymmetric presentation of glaucoma. The difference between perfusion pressure and IOP was much less in the right eye, which had the more advanced signs of glaucoma.
Figure 5.
 
Diurnal IOP and MOPP in a patient with an asymmetric presentation of glaucoma. The difference between perfusion pressure and IOP was much less in the right eye, which had the more advanced signs of glaucoma.
Table 1.
 
Diurnal Pressures
Table 1.
 
Diurnal Pressures
IOP SBP DBP MOPP MOPP-IOP
POAG 19.2 ± 5.0 128.6 ± 11.3 73.6 ± 8.4 42.0 ± 7.1 22.7 ± 11.0
NORMALS 13.0 ± 3.0 125.9 ± 13.6 73.4 ± 6.9 47.6 ± 6.1 34.7 ± 7.9
Table 2.
 
The Absolute and Percentage Diurnal Changes in IOP and MOPP
Table 2.
 
The Absolute and Percentage Diurnal Changes in IOP and MOPP
IOP Change (Absolute) IOP Change (Relative, %) MOPP Change (Absolute) MOPP Change (Relative, %)
uPOAG 10.3 ± 2.8 42 ± 11 19.2 ± 3.8 38 ± 7
Normals 6.8 ± 1.4 41 ± 7 14.4 ± 3.2 26 ± 5
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×