Ischemic stroke is the main cause of death and the most common cause of acquired physical disability worldwide. Recent demographic changes increase the relevance of stroke and its sequelae. The acute treatment for stroke is restricted to causative recanalization and restoration of cerebral blood flow, including both intravenous thrombolysis and mechanical thrombectomy. Still, only a limited number of patients are eligible for these time-sensitive treatments. Hence, new neuroprotective approaches are urgently needed. Neuroprotection is thus defined as an intervention resulting in the preservation, recovery, and/or regeneration of the nervous system by interfering with the ischemic-triggered stroke cascade. Despite numerous preclinical studies generating promising data for several neuroprotective agents, successful bench-to-bedside translations are still lacking. The present study provides an overview of current approaches in the research field of neuroprotective stroke treatment. Aside from “traditional” neuroprotective drugs focusing on inflammation, cell death, and excitotoxicity, stem-cell-based treatment methods are also considered. Furthermore, an overview of a prospective neuroprotective method using extracellular vesicles that are secreted from various stem cell sources, including neural stem cells and bone marrow stem cells, is also given. The review concludes with a short discussion on the microbiota–gut–brain axis that may serve as a potential target for future neuroprotective therapies.

Despite tremendous progress in modern-day stroke therapy, ischemic stroke remains a disease associated with a high socioeconomic burden in industrialized countries. In light of demographic change, these health care costs are expected to increase even further. The current causal therapeutic treatment paradigms focus on successful thrombolysis or thrombectomy, but only a fraction of patients qualify for these recanalization therapies because of therapeutic time window restrictions or contraindications. Hence, adjuvant therapeutic concepts such as neuroprotection are urgently needed. A bench-to-bedside transfer of neuroprotective approaches under stroke conditions, however, has not been established after more than twenty years of research, albeit a great many data have demonstrated several neuroprotective drugs to be effective in preclinical stroke settings. Prominent examples of substances supported by extensive preclinical evidence but which failed clinical trials are tirilazad and disodium 2,4-sulphophenyl-N-tert-butylnitrone (NXY-059). The NXY-059 trial, for instance, was retrospectively shown to have a seriously weak study design, a trial of insufficient quality and a poor statistical analysis, although it initially met the recommendations of the STAIR committee. In light of currently ongoing novel neuroprotective stroke trials, such as ESCAPE-NA, and to avoid the mistakes made in the past, an improvement in study quality in the field of stroke neuroprotection is urgently needed. In the present review, animal models closely reflecting the “typical” stroke patient, occlusion techniques and the appropriate choice of time windows are discussed. In this context, the STAIR recommendations could provide a useful orientation. Taking all of this into account, a new dawn for neuroprotection might be possible.

CCL11 has recently been shown to differentially affect cell survival under various pathological conditions including stroke. Indeed, CCL11 promotes neuroregeneration in neonatal stroke mice. The impact of CCL11 on the adult ischemic brain, however, remains elusive. We therefore studied the effect of ectopic CCL11 on both adolescent (six-week) and adult (six-month) C57BL6 mice exposed to stroke. Intraperitoneal application of CCL11 significantly aggravated acute brain injury in adult mice but not in adolescent mice. Likewise, post-stroke neurological recovery after four weeks was significantly impaired in adult mice whilst CCL11 was present. On the contrary, CCL11 stimulated gliogenesis and neurogenesis in adolescent mice. Flow cytometry analysis of blood and brain samples revealed a modification of inflammation by CCL11 at subacute stages of the disease. In adolescent mice, CCL11 enhances microglial cell, B and T lymphocyte migration towards the brain, whereas only the number of B lymphocytes is increased in the adult brain. Finally, the CCL11 inhibitor SB297006 significantly reversed the aforementioned effects. Our study, for the first time, demonstrates CCL11 to be a key player in mediating secondary cell injury under stroke conditions. Interfering with this pathway, as shown for SB297006, might thus be an interesting approach for future stroke treatment paradigms.

Objective: This study aims to assess the prevalence of clinically significant incidental findings as well as incidental findings of minor clinical significance in multiparametric MRI (mpMRI) of the prostate. Materials and Methods: A retrospective analysis was conducted on 607 male patients (mean age: 72 years) who underwent prostate MRI between 2018 and 2023 at a single center. Two radiologists reviewed in consensus the scans for incidental findings during multiparametric MRI of the prostate. The findings were classified according to their clinical relevance, organ group and patient age. Results: Among 607 male patients (mean age: 72 years), 665 incidental findings were identified in 410 patients (67.5%; 95% CI 63.7–71.1). This corresponds to an average of 1.10 incidental findings per patient across the entire cohort. Of the 665 findings, 12 (1.8%; 95% CI 0.9–3.1) were classified as clinically significant. These included cases of sarcoma, rectal carcinoma, hydronephrosis, aortic aneurysm, avascular necrosis of the femoral head and high-grade disc protrusion with spinal canal stenosis and diverticulitis. Conclusions: Our data indicate that incidental findings are common in prostate mpMRI examinations; however, only a small proportion are clinically significant. This underscores the need for awareness of such findings, while avoiding unnecessary follow-up for those without clinical relevance.

Ösophagusperforationen sind seltene, aber schwerwiegende Notfälle mit einer hohen Mortalität, die stark von Ursache und Behandlungszeitpunkt abhängt. Insbesondere spontane und iatrogene Perforationen gehen mit einer erheblichen Letalität einher, wobei eine verzögerte Therapie das Risiko weiter erhöht [1]. Mit der zunehmenden Anwendung endoskopischer Verfahren ist auch die Inzidenz von Ösophagusperforationen gestiegen, wobei iatrogene Verletzungen im Rahmen solcher Eingriffe die häufigste Ursache darstellen [2]. Spontane Rupturen, insbesondere beim Boerhaave-Syndrom, entstehen durch plötzliche Druckspitzen im Ösophagus, meist durch starkes, wiederholtes Erbrechen. Seltener sind traumatische Perforationen oder solche durch Fremdkörperingestionen, die aufgrund ihrer oft unspezifischen klinischen Symptomatik erhebliche diagnostische Herausforderungen darstellen. Die radiologische Bildgebung spielt eine zentrale Rolle bei der Diagnostik von Ösophagusperforationen. Während konventionelle Röntgenaufnahmen erste Hinweise auf eine Perforation liefern können, etwa in Form eines Mediastinalemphysems, weist die CT des Thorax je nach Studie eine hohe Sensitivität und Spezifität in der Detektion von Perforationen auf [3]. Typische Befunde umfassen Mediastinalemphyseme, Pleuraergüsse oder andere lokalisierte Luftansammlungen. Die Endoskopie hingegen ermöglicht sowohl die direkte Visualisierung der Läsion als auch minimal-invasive therapeutische Eingriffe. Im vorliegenden Fall führte das akzidentelle, unbemerkte Verschlucken eines scharfkantigen Tablettenblisters zu einer unspezifischen Symptomatik, die eine weitere Abklärung erforderte. Die ungewöhnliche Ursache sowie das Fehlen anamnestischer Hinweise machten den Fall diagnostisch besonders herausfordernd. Received: 12 February 2025 Accepted after revision: 27 May 2025 Article published online: 23 June 2025 © 2025. Thieme. All rights reserved. Georg Thieme Verlag KG Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany