Glaucoma has been referred to by many as a biomechanical disorder. After all, the optic nerve head (ONH) is exposed to high levels of biomechanical stress arising from various loads or pressures ‐ exhibiting constant fluctuations ‐ including, but not limited to: the intraocular pressure (IOP), the cerebrospinal fluid pressure (CSFP), the orbital fat pressure, the traction of the optic nerve (strongest in adduction), and stresses induced by diastole- to-systole choroidal expansion. Such stress levels are known to deform the ONH tissues; when they exceed their homeostatic range, they may be responsible (in part) for the development and progression of glaucoma. These effects could be exacerbated if stress levels directly alter blood flow, or in the presence of existing vascular dysfunction. Such interactions have not been studied in enough depth, and more clinical/engineering studies should be warranted.In this study, the authors aimed to measure (1) ocular rigidity (a 'global' quantity approximating the elasticity of the corneo-scleral shell); and (2) neuroretinal damage (assessed through RNFL thickness) in patients with vasospasticity or atherosclerosis. Why vasospastic patients? Firstly, it has been shown that vasospasticity is a risk factor for glaucoma. Secondly, evidence suggests that patients with vasospasticity could exhibit ocular blood flow dysregulation in response to biomechanical stimuli. Overall, the authors hypothesized that lower values of ocular rigidity (i.e., more ocular tissue deformations in response to IOP elevations) should correlate with greater glaucoma damage (as assessed through OCT-based RNFL thickness measurements). From their results, the authors were able to confirm their hypothesis but the correlation was only significant for the infero-temporal region. No such correlations were observed in the atherosclerotic group. The authors concluded that more structural damage could potentially occur in eyes that are less rigid and in the presence of vasospasticity. These results could potentially suggest strong interactions between ocular tissue biomechanics and vascular dysfunction that could yield glaucomatous damage.Several limitations in this pilot study were well acknowledged by the authors. Firstly, the sample size was small (ten vasospastic and 37 atherosclerotic participants), and the authors would benefit from reproducing their work in a much larger cohort. Second, the presence of vascular disorders was only assessed through patient questionnaires, and more quantitative tools (e.g., blood flow measurements) should naturally be used to confirm vascular dysfunction. In addition, a wider spectrum of subjects should be considered, and also those with no vascular dysfunction, as atherosclerosis may well be stiffening the nerve.
The measurement of ocular rigidity may have its own limitation
It is also worth noting that the measurement of ocular rigidity may have its own limitation. Ocular rigidity is basically defined as how a change in ocular volume (loosely defined) would result in a change in IOP. Ocular rigidity has been suggested to reflect the biomechanical properties of the sclera. Mathematical modelling tells us that a higher ocular rigidity is linked to a stiffer sclera, but not in the presence of a higher baseline IOP, thus contradicting previous thinking. 1 In addition, ocular rigidity will not be able to reflect the robustness (or fragility) of a local region (such as the ONH), and other methods need to be developed to assess ONH robustness.2 Nevertheless, ocular rigidity may still represent a clinically viable parameter, especially if could be assessed non-invasively. In previous publications, the authors found an elegant way to assess ocular rigidity in vivo noninvasively using OCT imaging the choroid during the cardiac cycle, and measurements of the ocular pulse amplitude.3 Their technique was validated against measurements obtained with a more traditional method.4 It was employed in the proposed study to assess ocular rigidity in vasospastic patients.Overall, the proposed study has the merit of bridging the gap (from a clinical point-of-view) between two critical physical phenomena that are known to interact in the eye and that may well be driving glaucomatous damage: soft tissue biomechanics and hemodynamics. As stated in the title, this study remains a pilot study, but it could hopefully encourage more engineering and clinical developments to better understand these interactions.
This study remains a pilot study, but it could hopefully encourage more engineering and clinical developments to better understand these interactions