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To assess the long-term outcome of Trabectome surgery in the treatment of primary open angle glaucoma (POAG) and pseudoexfoliative glaucoma (PEX): 3-year results. Trabectome surgery (NeoMedix, Tustin, CA, USA) was performed in 268 POAG patients (women 57.46%, men 42.54%, age 72.35 ± 9.63 years) and 98 PEX glaucoma patients (women 58.16%, men 41.84%, age 73.42 ± 8.54 years), and uncontrolled intraocular pressure (IOP). Parameters were examined preoperatively, 1 day, 6 weeks, 3, 6, 12, 24 and 36 months post surgery. Kaplan-Meier analysis was performed using Criteria A (IOP ≤ 21 mmHg or ≥20% reduction from preoperative IOP), Criteria B (IOP ≤ 18 mmHg or ≥20% IOP reduction), Criteria C (IOP ≤ 21 mmHg, with or without medication) and D (IOP ≤ 18 mmHg, with or without medication). Complete success was defined as IOP ≤ 21 mmHg (Criteria E) and IOP ≤ 18 mmHg without medication (Criteria F). IOP was reduced from 19.10 ± 4.11 mmHg to 14.27 ± 2.93 mmHg (p

Inflammatory changes have been postulated to contribute to secondary brain injury after aneurysmal subarachnoid hemorrhage (SAH). In human specimens after SAH as well as in experimental SAH using mice, we show an intracerebral accumulation of inflammatory cells between days 4 and 28 after the bleeding. Using bone marrow chimeric mice allowing tracing of all peripherally derived immune cells, we confirm a truly CNS-intrinsic, microglial origin of these immune cells, exhibiting an inflammatory state, and rule out invasion of myeloid cells from the periphery into the brain. Furthermore, we detect secondary neuro-axonal injury throughout the time course of SAH. Since neuronal cell death and microglia accumulation follow a similar time course, we addressed whether the occurrence of activated microglia and neuro-axonal injury upon SAH are causally linked by depleting microglia in vivo. Given that the amount of neuronal cell death was significantly reduced after microglia depletion, we conclude that microglia accumulation inflicts secondary brain injury after SAH.

This study was performed in order to evaluate the incidence of radiation retinopathy and optic neuropathy occurring after proton beam therapy for uveal melanoma. Included in this study were all patients who had been treated with primary proton beam therapy for uveal melanoma at the oncology service between May 1998 and June 2014 with a minimum follow-up of 12 months. Excluded were all patients who underwent re-irradiation, or vitrectomy due to exudative retinal detachment or for tumor-resection. During this period, 1127 patients matched the inclusion criteria, of whom 768 (68.1 %) and 463 (41.0 %) developed radiation retinopathy and optic neuropathy after a median time of 18.9 months (2.0–99.84 months) and 19.8 months (0.2–170.4 months), respectively. Mean follow-up was 53.4 months (12–170.4 months). Included were 558 men (49.5 %) and 569 women (50.5 %). Mean age was 61 years (16–89 years). Visual acuity slightly decreased from initial levels of 0.3 logMAR–0.4 logMAR in patients without developing any radiation-induced complication but severely decreased to 1.0 logMAR or 1.5 logMAR in the case of developing radiation retinopathy only or optic neuropathy, respectively. Independent risk factors for radiation retinopathy were a centrally (