Both invasive and noninvasive methods of estimating
E have been described in the literature. The invasive method involves injecting a known volume of liquid into the eye (Δ
V) and measuring the subsequent increase of IOP (ΔIOP); the curve of pressure-volume relationship is plotted and the coefficient of rigidity (E) is calculated based on the Freidenwald's equation.
3,4 The noninvasive method benefits from the fact that each cardiac cycle brings a bolus of blood into the ocular circulation. This inflow of blood (Δ
V) subsequently increases the IOP (ΔIOP), which is called ocular pulse amplitude (OPA) or pulse amplitude (PA). OPA can be easily measured with a pneumotonometry or a dynamic contour tonometry. The difficulty in a noninvasive method of estimating ocular rigidity is in the estimation of Δ
V, which is mostly the result of the pulsatile component of choroidal blood flow.
5 In the article by Hommer et al., they used fundus pulse amplitude (FPA) as Δ
V, which measures the movement between the cornea and inner retina in response to the cardiac pulse.
6 Ebneter et al. pharmacologically reduced IOP using acetazolamide (ΔIOP) and measured the change in axial length following the reduction of IOP (Δ
V).
7 They compared the amount of reduction in axial length (AL) between individuals who have achieved the same amount of IOP reduction; individuals with greater AL reduction were considered as having lower rigidity. Both noninvasive methods, using either FPA or AL, estimated ΔV by measuring the anterior to posterior expansion of the corneoscleral shell, which is itself dependent on the ocular rigidity, the preexisting volume of the choroidal circulation, and the preexisting IOP level.
8 It may, therefore, be more pertinent to use a variable that indicates the amount of blood injected into the eye with each cardiac cycle as an indicator of Δ
V rather than a variable indicating the response of ocular coat to an increase in volume.