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Br J Ophthalmol. 2007 April; 91(4): 405–406.
PMCID: PMC1994757

Retinal vein pulsation predicts increasing optic disc excavation

Short abstract

Spontaneous retinal vein pulsation in glaucoma

Several factors are associated with glaucoma progression, most notably elevated intraocular pressure (IOP), age, stage of the disease and presence of optic disc haemorrhages.1,2,3,4 In this issue of the British Journal of Ophthalmology, Balaratnasingam et al5(see page xxx) describe a new factor associated with glaucoma progression—that is, the ophthalmodynamometric force (ODF) necessary to induce central or hemiretinal vein pulsation. In their study, baseline ODF, measured in subjects with glaucoma or suspects of having glaucoma, predicted increased optic disc excavation determined by masked assessment of optic disc stereophotography (average of 82 months of follow‐up). The same group of investigators have previously shown that approximately 50% of patients with glaucoma have spontaneous venous pulsation (SVP), compared to 98% of age‐matched normal controls,6 which was confirmed in other cohorts.7,8 Moreover, a strong inverse correlation was observed between the ODF and the mean deviation of the visual field. In cases where different ODF was required to induce pulsation of the two hemi‐veins, there was a strong association between differences in the ODF measured in the two veins and differences in the corresponding hemifield mean sensitivities.6,7 These findings suggest that determining the presence of SVP and measuring ODF in cases without SPV might be clinically relevant in glaucoma and certainly deserves further research.

Despite some controversy regarding the aetiology of SVP, it is generally believed that it is caused by the oscillation of IOP during the cardiac cycle at a level significantly higher than the pressure in the retrolaminar portion of the central retinal vein.9,10,11 Several factors are known to influence the venous pulsation pressure (VPP), which is the minimum IOP necessary to induce venous pulsation, consequently, the presence of SVP. Increased cerebrospinal fluid (CSF) pressure and increased systemic blood pressure cause an increase in VPP.7,9,10 This is observed clinically by the common absence of SVP in patients with elevated CSF pressure. Additionally, evidence from modelling experiments suggest that the increased arterial resistance before the venous system reduces VPP, and the increased venous resistance increases VPP.9

A very intriguing question is why does VPP increase in individuals with glaucoma? It is unlikely that CSF pressure increases in individuals with glaucoma. Systemic hypertension is weakly associated with glaucoma,12,13 but previous studies have shown that the venous pulsation findings in subjects with glaucoma are independent of blood pressure.7 Several studies have shown that arterial resistance is increased in glaucoma, probably early in the course of the disease, which would cause a reduction and not an increase in VPP.14,15 Therefore, the most likely explanation for an increased VPP in subjects with glaucoma is an increase in central retinal vein resistance as it exits the eye. This increased resistance could certainly help explain the higher risk of central and hemiretinal vein occlusions observed in subjects with glaucoma.16,17 It could also help explain another common vascular phenomenon observed in subjects with glaucoma, namely the occurrence of optic disc haemorrhages.1,2 The aetiology of optic disc haemorrhages is still controversial,18 but increased venous resistance could certainly contribute to its occurrence. It would be interesting to compare the ODF in individuals with and without optic disc haemorrhages, but unfortunately the study of Balaratnasingam et al was not adequately powered for that analysis.

It is not difficult to imagine why central retinal vein resistance would be increased in glaucoma, when we consider the significant changes that occur at the level of the optic nerve head and, particularly, at the lamina cribrosa as glaucomatous cupping develops.19,20,21 The posterior displacement of the lamina cribrosa associated with nasalisation of the vessels in the optic disc can cause disturbances in blood flow in the central retinal vein, ultimately leading to increased resistance. The fact that this higher venous resistance, in the form of a higher ODF, predicts increased excavation is, however, very intriguing. This group of investigators have shown that ODF is strongly correlated with visual field mean deviation, and, therefore, could be considerer as an epiphenomenon of more advanced stages of the disease.7 The fact, however, that ODF predicts increased excavation after adjustment for visual field mean deviation, and for other variables such as age and IOP, suggests that increased VPP might be in fact an independent factor contributing to glaucoma progression.

In the study of Balaratnasingam et al, subjects with glaucoma and suspects of having glaucoma were grouped together. It would be interesting if the authors had reported on the predictive value of ODF in these two groups separately. Since, in their original studies, 75% of glaucoma suspect individuals have SVP, and an arbitrary ODF value of zero was utilised in these subjects, it is expected a low predictive value of ODF in this group due to this truncated effect. Ophthalmodynamometry is a relatively cumbersome technique that is unlikely to be readily incorporated into clinical practice for glaucoma. Determining the presence of SVP, however, is much simpler and can easily be performed during routine examination of optic discs. Balaratnasingam et al showed that increased excavation was two times more frequent in patients without SVP than in those with SVP (28% vs 14%, respectively) and, therefore, the mere determination of presence of SVP can be clinically helpful. Here, again, it would be useful to know the predictive value of the absence of SVP for increasing excavation in the two groups of patients, separately. It would be particularly useful to know the proportion of conversion that occurred in the 25% of suspects of glaucoma, who did not have SVP at baseline.

The study of Balaratnasingam et al certainly generates several interesting hypothesis on the role of altered venous resistance in glaucoma and should lead to further studies in this otherwise relatively neglected side of the vascular blood supply in glaucoma. Meanwhile, based on the data presented, clinicians should be encouraged to observe the presence of SVP in their patients, which could indicate a lower risk for glaucomatous progression. For those patients without SVP, measurement of ODF, although technically more complicated, might be a valuable clinical tool.

Footnotes

Competing interests: None declared.

References

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