Ocular rigidity and neuroretinal damage in patients with vasospasticity: a pilot study.

OBJECTIVE

Evidence suggests that ocular blood flow dysregulation in patients with vasospasticity could occur in response to biomechanical stimuli, contributing to optic nerve head susceptibility in glaucoma. We evaluate the role of vasospasticity in the association between ocular rigidity (OR) and neuroretinal damage, hypothesizing that low OR correlates with greater glaucoma damage in patients with vasospasticity.

DESIGN

Cross-sectional study.

PARTICIPANTS

Patients with open-angle glaucoma (OAG), suspect discs, or no glaucoma.

METHODS

OR was measured using a noninvasive, validated method developed by our group. Retinal nerve fibre layer (RNFL) and ganglion cell complex thicknesses were acquired using spectral domain optical coherence tomography. Vasospasticity was assessed by a standardized questionnaire that was based on existing validated questionnaires and adapted to our requirements. Atherosclerosis was evaluated based on Broadway and Drance's (1998) cardiovascular disease score. Correlations between OR and structural parameters were assessed in patients with vasospasticity and those with atherosclerosis.

RESULTS

Of 118 patients with either OAG (n = 67), suspect discs (n = 26), or no glaucoma (n = 25) who were recruited consecutively, 10 were classified as having vasospasticity, and 37 as having atherosclerosis. In the vasospastic group, significant correlations were found between OR and the minimum ganglion cell complex thickness (rs = 0.681, p = 0.030), the average RNFL thickness (rs = 0.745, p = 0.013), and the RNFL in the temporal quadrant (rs = 0.772, p = 0.009), indicating more damage with lower OR. Similar trends were maintained when applying multiple testing correction; however, only the eighth RNFL clock hour corresponding to the inferior-temporal peripapillary region remained significantly correlated with OR in the vasospastic group (p = 0.015). In contrast, no correlation was found in the atherosclerotic group (p > 0.05).

CONCLUSIONS

The findings of the current pilot study indicate a trend for more neuronal structural damage in less-rigid eyes of patients with vasospasticity, meaning that OR may play a greater role in glaucoma in vasospastic patients than in patients with atherosclerosis. Although these results provide interesting insight into the pathophysiology of OAG, further investigation is needed to confirm our observations.