Richard Stodtmeister

Ocular perfusion pressure in glaucoma

This review article discusses the relationship between ocular perfusion pressure and glaucoma, including its definition, factors that influence its calculation and epidemiological studies investigating the influence of ocular perfusion pressure on the prevalence, incidence and progression of glaucoma. We also list the possible mechanisms behind this association, and discuss whether it is secondary to changes in intraocular pressure, blood pressure or both. Finally, we describe the circadian variation of ocular perfusion pressure and the effects of systemic and topical medications on it. We believe that the balance between IOP and BP, influenced by the autoregulatory capacity of the eye, is part of what determines whether an individual will develop optic nerve damage. However, prospective, longitudinal studies are needed to better define the role of ocular perfusion pressure in the development and progression of glaucoma.

Pressure compliance of the optic nerve head in low tension glaucoma.

Twenty eyes of 10 healthy subjects, 11 eyes of seven patients with low tension glaucoma, and three eyes of three patients with ischaemic optic neuropathy were investigated. Visual evoked responses were recorded under stepwise artificially increased intraocular pressures. The results of the visual evoked response recording (pressure compliance test) allow a clear distinction to be made between healthy subjects, patients with low tension glaucoma, and patients with ischaemic optic neuropathy. In the groups investigated a lack of autoregulation of the optic nerve head circulation was found in patients with low tension glaucoma only. Patients with anterior ischaemic optic neuropathy showed the same pressure compliance behaviour as healthy subjects. The methods used here seem to provide a practicable clinical tool in the differential diagnosis of low tension glaucoma.

Comparison of Apraclonidine and Timolol in Chronic Open-angle Glaucoma: A Three-month Study

PURPOSE To compare the safety and efficacy of apraclonidine ophthalmic solution 0.25% and 0.5% (both given 3 times daily) to timolol maleate (0.5%) given twice daily, in primary open-angle glaucoma or ocular hypertension. METHODS This study was a 90-day prospective, multicenter, double-masked, randomized, parallel group trial. Intraocular pressure (IOP) measurements were made between 8:00 and 10:00 AM before the morning dose (i.e., up to 12 hours after the evening dose of glaucoma medication) and at 4:00 PM (i.e., 8 hours after the morning dose of glaucoma medication). Patients with off-therapy IOP of greater than 22 mmHg and less than 35 mmHg were entered into the study and were assessed 14, 30, and 90 days after treatment. RESULTS Sixty-nine patients were enrolled; there were no significant demographic differences among the three study groups. All three treatments significantly reduced IOP over 90 days (P < 0.011). For apraclonidine 0.5%, IOP reductions from 25.8 +/- 3.2 mmHg (pretreatment) to 20.4 +/- 4.00 mmHg (day 90) were observed; for apraclonidine 0.25%, from 25.7 +/- 3.05 mmHg (pretreatment) to 22.1 +/- 4.24 mmHg (day 90); and for timolol 0.5% from 26.1 +/- 3.79 mmHg to 21.1 +/- 5.91 mmHg (day 90). The 90-day period of therapy was completed by 12 patients treated with apraclonidine 0.5%, 21 patients treated with apraclonidine 0.25%, and 23 patients treated with timolol 0.5%. There were no serious adverse events. Fourteen of 22 patients (0.5% apraclonidine) and 21 of 23 patients (0.25% apraclonidine) tolerated the drug well; ocular allergy developed in the remaining patients treated with apraclonidine, which resolved upon discontinuation. CONCLUSIONS Apraclonidine effectively lowers IOP associated with open-angle glaucoma or ocular hypertension; these pilot results will need to be confirmed by a larger pivotal study. Long-term therapy for some patients may be inhibited by ocular allergy for which there was a higher incidence to the 0.5% apraclonidine solution than to the 0.25% solution in this study. Apraclonidine may be of value as an additional therapy for open-angle glaucoma in selected patients.

The effect of caffeine on retinal vessel diameter in young healthy subjects.

Purpose:  To investigate the effect of caffeine on retinal vessel diameter before and during flicker light stimulation in young healthy subjects.

Enhanced pressure in the central retinal vein decreases the perfusion pressure in the prelaminar region of the optic nerve head.

PURPOSE The pressure in the central retinal vein (CRVP) has been shown to be higher in glaucoma patients than in controls. Until now, these measurements have been performed in arbitrary units or in units of ophthalmodynamometric force. In our study, a contact lens dynamometer, calibrated in mm Hg, was used to calculate the retinal perfusion pressure. METHODS A total of 27 patients with primary open angle glaucoma (POAG) and 27 healthy control subjects were included in the study. The IOP measurement included Goldmann applanation tonometry, whereas the pressure enhancement measurement consisted of contact lens dynamometry. results: the pressures are given in mm hg, and are expressed as the mean ± SD for the control subjects versus the POAG patients: IOP 14.4 ± 2.7 vs. 15.4 ± 2.9, systolic blood pressure 141 ± 20.1 vs. 153 ± 16.5 (P = 0.013), central retinal vein threshold pressure (CRVTP) 11.9 ± 3.8 vs. 16.8 ± 5.0, CRVP 15.0 ± 2.7 vs. 17.9 ± 4.2, and retinal perfusion pressure (PPret) standard 84 ± 12.2 vs. 94 ± 9.1 and new 83 ± 12.2 vs. 91 ± 9.6. The differences in PPret between using the new versus the standard method are 0.55 ± 1.33 vs. -2.5 ± 3.89 (P = 0.041 and P = 0.002, respectively). The PPret was at least 5.0 mm Hg lower in 5 of the 27 POAG patients when the new calculation method was used. CONCLUSIONS The perfusion pressure in the retina and prelaminar region of the optic nerve head (ONH) may be lower than expected because the CRVP may be higher. The pressure measurement in the central retinal vein may be a step toward a better understanding of ONH pathophysiology.

Simultane Ableitung von VECP und Muster-ERG bei künstlicher Erhöhung des Augeninnendrucks

The visual evoked cortical potentials (VECP) are changed by the artificial increase in intraocular pressure (IOP). The exact location of the damage is still unclear. One possibility is that the increa

Diameter of retinal vessels in patients with diabetic macular edema is not altered by intravitreal ranibizumab (lucentis).

Purpose: To investigate the effect(s) of intravitreally injected ranibizumab on retinal vessel diameter in patients with diabetic macular edema. Methods: Participants of this prospective study were 14 men and 16 women (30 eyes) aged 60 ± 11 years (mean ± standard deviation), all with clinically significant diabetic macular edema. Treatment comprised 3 intravitreal injections of ranibizumab given at 4-week intervals. Examinations were conducted before the first (baseline), before the second (Month 1), before the third (Month 2) injections, and 3 months after baseline (Month 3). Measured parameters included systemic blood pressure, static retinal vessel analysis (central retinal artery equivalent and central retinal vein equivalent), and dynamic retinal vessel analysis, as measured by the change in vessel diameter in response to flicker stimulation during three measurement cycles. Flicker stimulation was accomplished using a 50-second baseline recording, followed by an online measurement during 20-second flicker stimulation and 80-second online measurements in both arteriolar and venular vessel segments. Results: Static retinal vessel analysis showed a reduction of central retinal artery equivalent from 186.25 ± 51.40 &mgr;m (baseline) to 173.20 ± 22.2 &mgr;m (Month 1), to 174.30 ± 27.30 &mgr;m (Month 2), and to 170.56 ± 22.89 &mgr;m (Month 3), none of which was statistically significant (P = 0.23, 0.12, and 0.14, respectively). Central retinal vein equivalent was reduced from 216.21 ± 25.0 &mgr;m (baseline) to 214.48 ± 25.4 &mgr;m (Month 1), to 214.80 ± 24.30 &mgr;m (Month 2), and to 211.41 ± 24.30 &mgr;m (Month 3), revealing no statistically significant differences between examination time points (P = 0.54, 0.06, and 0.24, respectively). Dynamic vessel analysis yielded a mean retinal arterial diameter change of +1.47% ± 2.3 (baseline), +1.91% ± 2.5 (Month 1), +1.76% ± 2.2 (Month 2), and +1.66% ± 2.1 (Month 3), none of which showed statistically significant differences (P = 0.32, 0.49, and 0.70, respectively). Mean retinal venous diameter changes were +3.15% ± 1.7 (baseline), +3.7% ± 2.3 (Month 1), +4.0% ± 2.0 (Month 2), and +4.95% ± 1.9 (Month 3), none of which showed statistically significant differences (P = 0.12, 0.17, and 0.14, respectively). Central retinal thickness, as measured by spectral domain optical coherence tomography, decreased significantly from 435.2 ± 131.8 &mgr;m (baseline) to 372.3 ± 142.8 &mgr;m (Month 3), P = 0.01. Regression analysis of arteriolar and venular diameters indicated that there was no significant correlation between these 2 parameters (r = 0.053; P = 0.835 and r = 0.06; P = 0.817, respectively). Also, no significant correlation was observed between the difference in the central retinal thickness and change in arteriolar or venular dilatation (r = 0.291, P = 0.241 and r = 0.06, P = 0.435, respectively). Conclusion: Intravitreally applied ranibizumab did not significantly affect retinal vessel diameter in patients with diabetic macular edema. Decline in the central foveal thickness after ranibizumab therapy, as measured by spectral domain optical coherence tomography, was not linked to any change in retinal vessel diameter or dilatatory response, neither for arterioles nor venules.

Central retinal venous pulsation pressure in different stages of primary open-angle glaucoma

Background To evaluate the central retinal venous pulsation pressure (CRVPP) in patients with intraocular pressure (IOP)-controlled early, moderate and advanced open-angle glaucoma and a healthy control group. Methods CRVPP was measured with a contact lens dynamometer calibrated in mm Hg (Meditron GmbH, Voelklingen, Germany) in 34 patients with IOP-controlled open-angle glaucoma who were selected consecutively and according to the stage of their visual fields and 27 age-matched healthy controls. If a spontaneous venous pulsation was seen, CRVPP was considered to be equal to IOP. Visual fields were tested with the Humphrey 30-2 SST programme. The ocular perfusion pressure was conventionally calculated as OPP1=2/3MAP − IOP (MAP=systemic mean arterial blood pressure) and, using the measured CRVPP in the formula, as OPP2=2/3MAP − CRVPP. Statistical analysis was performed using the Kruskal–Wallis and the Mann–Whitney U test. Results Median CRVPP was 14.0 mm Hg (IQR 12.0–16.0) in controls, 15.0 mm Hg (IQR 14.0–17.0) in early, 38.9 mm Hg (IQR 29.9–48.4) in moderate and 34.6 mm Hg (IQR 23.9–51.0) in advanced glaucoma cases. The conventionally calculated OPP1 was 49.8 mm Hg (IQR 42.7–57.6) for controls, 56.9 mm Hg (IQR 55.3–58.8) for early, 56.6 mm Hg (IQR 51.2–64.4) for moderate and 59.3 mm Hg (IQR 53.9–61.6) for advanced cases. OPP2 was equal to OPP1 in the control group, 56.1 mm Hg (IQR 54.5–57.9) in early, 25.1 mm Hg (IQR 15.7–38.6) and 34.2 mm Hg (IQR 20.4–47.5) in moderate and advanced cases. This difference was statistically significant for moderate (OPP2 lower; p=0.003) and advanced (OPP2 lower; p=0.002) cases. Conclusions In more advanced cases of glaucoma, CRVPP seems to be much higher than previously thought. This might further compromise the perfusion pressure in the prelaminar region of the optic nerve head and be of clinical importance, especially in IOP-controlled more advanced cases. This should be considered as a possible risk factor for progression. Trial registration number ClinicalTrials.gov ID: NCT01503996.

The short‐term effect of flavonoid‐rich dark chocolate on retinal vessel diameter in glaucoma patients and age‐matched controls

To investigate the effect of flavonoid‐rich dark chocolate and non‐flavonoid‐rich white chocolate on retinal vessel diameter in glaucoma patients and age‐matched controls.

Contact Lens Dynamometry: The Influence of Age

PURPOSE To examine the influence of age on systolic (systOAP) and diastolic (diastOAP) blood pressure in the ophthalmic artery (OA) measured by a new contact lens dynamometer (CLD). METHODS In a prospective cross-sectional clinical trial, 106 eyes of 106 patients (58 women, 48 men) were examined. A nearly uniform age distribution was achieved by recruiting subjects in seven age groups, with at least 12 in each decade. Blood pressure in the OA was measured with a new CLD. Arterial blood pressure at the upper arm was measured by cuff, according to the Riva-Rocci (RR) METHOD: Main outcome measures were: SystOAP and diastOAP in the OA and systolic (systRR) and diastolic (diastRR) pressures in the subclavian artery. RESULTS The blood pressures showed the following linear regression equations in association with age: systRR (mm Hg) = 115 + 0.45 × age (years) (R = 0.50; P < 0.00001); diastRR (mm Hg) = 72 + 0.28 × age (years) (R = 0.42; P < 0.00001); systOAP (mm Hg) = 61 + 0.93 × age (years) (R = 0.74; P < 0.0001); and diastOAP (mm Hg) = 44 + 0.37 × age (years) (R = 0.57; P < 0.0001). CONCLUSIONS The relative slopes of the regression lines relating age to diastolic and systolic pressures are steeper in the ophthalmic than in the subclavian artery, indicating that the pressures in the ophthalmic artery increase faster with age than do the associated pressures in the subclavian artery, as measured by the standard sphygmomanometry. This phenomenon may be explained by progressive stiffening of the walls in the carotid and ophthalmic arteries. The effect of age should be taken into account whenever interpreting ophthalmodynamometric measurements for clinical diagnostic purposes.