Although the eye is the only organ in the body in which blood vessels are readily visible, a technique for the accurate and reproducible measurement of ocular blood flow and its component parts has proved elusive.1 The increasing likelihood of a multifactorial pathogenesis for glaucoma and possible importance of optic nerve head perfusion in the pathogenesis of glaucoma has added impetus to the search for a clinical method of measuring ocular blood flow.

The pulsatile variation in ocular pressure results from flow of blood into the eye during cardiac systole. First recorded in 1850 by Wegner,2 various methods have been tried to record the pulsatile variation in intraocular pressure. Langham and co-workers3 adapted the pneumotonometer to measure intraocular pressure every 30 ms thus obtaining an accurate record of the pulsatile change in pressure. They hypothesised that the pressure pulse could be converted into a volume pulse using the known relation between ocular pressure and ocular volume. By multiplying this volume by the heart rate a measure of pulsatile ocular blood flow (POBF) could be obtained. The instrument has been developed and measurements are easily and quickly performed and the reproducibility is acceptable.4 5

There are, as with all techniques, problems. Knowledge of these limitations is essential if the results of studies are to be interpreted correctly. The conversion of the pressure pulse to a volume pulse relies on limited data and will be affected by scleral rigidity and ocular volume (proportional to the axial length of the eye). Only the pulsatile component of flow is assessed and the ratio of pulsatile to non-pulsatile flow may change with alteration in the heart rate, intraocular pressure or systemic blood pressure, and a change in the compliance of the blood vessels. From this index of global ocular blood flow (largely choroidal supplied by the posterior ciliary vessels) any inference about the optic nerve head circulation, which contributes but a tiny part to total ocular blood flow, must be carefully drawn.

One must also try to distinguish between the usefulness of a technique in determining differences between groups of patients and normal controls, or groups of patients on and off treatment and its usefulness in providing clinically relevant information in an individual patient.

Fontana et al (p 731) provide an extensive normal database for POBF measurement in a normal population and also measure POBF in patients with normal tension glaucoma. The results confirm previous studies finding POBF to be reduced in these patients.6 They also report a statistically significant difference in pulsatile ocular blood flow in the affected eye compared with the unaffected eye in patients with “unilateral” normal tension glaucoma. This finding is new and intriguing. Many of the limitations of the technique do not apply in this circumstance. There was no difference in axial length between the eyes. Intraocular pressure was slightly higher in the affected eye although the difference would have only a small effect on perfusion pressure. Systemic variables of blood pressure and heart rate are identical. Unless one proposes that there is a difference in scleral rigidity between the two eyes it appears that the difference in POBF is real and provides further evidence for the importance of compromised ocular perfusion in the pathogenesis of glaucoma. The rider about scleral rigidity is important, for although very unlikely in this study, a reduced scleral rigidity would both reduce the calculated POBF and might make the optic nerve head more susceptible to pressure damage.

On a broader plain it is still unclear whether measurement of ocular blood flow will aid the diagnosis and treatment of glaucoma. Ocular pulse analysis currently provides the easiest and most clinically acceptable means of deriving an index of ocular blood flow, albeit that there are the significant problems discussed earlier. The range in POBF values in both normal and abnormal eyes makes a clear separation of the normal from the abnormal on an individual basis extremely difficult, but this is also increasingly true of measurement of intraocular pressure. A combination of the two measurements, which the technique gives, might provide us with additional information to aid diagnosis and monitor the effect of therapy. Great ingenuity has been shown in the many methods devised to record the pulsatile change in ocular pressure; it may prove that harnessing this record correctly, with full knowledge of its limitations, provides a good deal more information than a simple pressure measurement.