Zeitz Oliver

Gollrad Johannes, Böker Alexander, Vitzthum Sebastian, Besserer Angela, Heufelder Jens, Gauger Ulrich et al.

Proton therapy effectively treats iris melanoma with low recurrence/metastasis. However, large treatment fields (over 10 clock hours) significantly increase secondary glaucoma and vision loss risk.

Riechardt Aline I, Stroux Andrea, Seibel Ira, Heufelder Jens, Zeitz Oliver, Böhmer Dirk et al.

This study found that for choroidal melanoma proton therapy, the radiation dose to the optic disc, not the irradiated optic nerve length, is the primary predictor for secondary glaucoma and other severe ocular complications.

Costa Vital P, Harris Alon, Anderson Douglas, Stodtmeister Richard, Cremasco Fernanda, Kergoat Helene et al.

This review highlights ocular perfusion pressure's role in glaucoma development and progression, suggesting the balance between eye pressure and blood pressure is key to optic nerve health.

Brown David M, Heier Jeffrey S, Clark W Lloyd, Boyer David S, Vitti Robert, Berliner Alyson J et al.

Intravitreal aflibercept significantly improved vision in CRVO-related macular edema, with benefits maintained at one year with PRN dosing, offering an effective treatment option.

Zeitz Oliver, Mayer Jeannette, Hufnagel Doreen, Praga Ralf, Wagenfeld Lars, Galambos Peter et al.

This study found healthy eyes show neurovascular coupling (blood flow increase with activity) in optic nerve arteries, but glaucomatous eyes do not, suggesting impaired vascular regulation in glaucoma.

Zeitz Oliver, Wagenfeld Lars, Wirtz Nick, Galambos Peter, Matthiesen Natalya, Wiermann Anne et al.

This study found oxygen free radicals induce transient contractions in isolated ciliary arteries, mimicking vasospasms. This suggests oxidative stress may contribute to glaucoma-related vascular dysfunction.

Galambos Peter, Vafiadis Joanna, Vilchez Silvia E, Wagenfeld Lars, Matthiessen Eike T, Richard Gisbert et al.

Glaucoma patients (NTG, POAG) showed compromised ocular blood flow autoregulation after postural change, unlike healthy controls. This insufficient compensatory response, particularly accelerated SPCA flow, suggests a potential glaucoma pathogenesis factor.