Wilhelm Küker

Die Creutzfeld-Jakob-Krankheit (CJK) ist eine seltene, durch Prionen (infektiöse Proteine) verursachte neurodegenerative Erkrankung. Prionen entstehen durch eine Konformationsänderung von normalen Proteinen (PrP^C) auf der Oberfläche von Neuronen. Diese pathologischen Proteine (PrP^Sc) verursachen eine Kettenreaktion durch die induzierte Konformationsänderung weiterer, bisher normaler Proteine. Received: 29 December 2025 Accepted after revision: 09 January 2026 Article published online: 11 February 2026 © 2026. Thieme. All rights reserved. Georg Thieme Verlag KG Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany

Die Hämophagozytische Lymphohistiozytose (HLH), auch Makrophagenaktivierungssyndrom (MAS) genannt, ist eine seltene Störung des Immunsystems mit überschießender systemischer Entzündungsreaktion und konsekutiver multifokaler Gewebedestruktion. Die Überstimulation von Makrophagen wird durch eine Unterfunktion von zytotoxischen T-Zellen und natural killer (NK)-Zellen hervorgerufen. Diese sind dann nicht mehr in der Lage, auslösende Antigene zu eliminieren und damit die gegen sie gerichtete Immunreaktion zu beenden. Received: 13 January 2025 Accepted after revision: 24 March 2025 Article published online: 25 April 2025 © 2025. Thieme. All rights reserved. Georg Thieme Verlag KG Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany

A 28-mm diameter and partially thrombosed intracranial aneurysm was found in a 10-year-old boy on an MRI for non-specific headaches. The large neck incorporated the left internal carotid artery (ICA) termination and proximal middle cerebral artery. Treatment was planned to prevent further growth and rupture. Because of the difficult anatomy, a braided stent was first placed across the aneurysm neck as a scaffold to allow for the placement of a flow-diverting stent after its endothelialisation. However, severe stent-induced endothelial hyperplasia was encountered when the flow diverter was inserted. This resulted in a transient ICA occlusion during the procedure before flow was restored by angioplasty. As a result, the patient suffered a mild transient dysphasia but permanent loss of vision in the left eye. All antiplatelet medications were stopped 1 year after the procedure without problem. The aneurysm has remained fully occluded in the 7 years since.

Brain imaging done as part of standard care may have clinical utility beyond its immediate indication. Using delirium as an exemplar, we determined the predictive value of baseline brain imaging variables [white matter changes (WMC) and atrophy] for delirium risk on long-term follow-up after transient ischemic attack (TIA)/stroke in a population-based cohort study. surviving TIA/stroke participants in the Oxford Vascular Study (OXVASC) were assessed prospectively for delirium during all hospitalisations over 6 months (2013–14). Using logistic regression, independent associations were determined between baseline OXVASC computed tomography or magnetic resonance brain imaging measures of WMC and cerebral atrophy (none/mild versus moderate/severe) and delirium adjusted for age, sex, baseline stroke severity, depression, illness severity and pre-admission cognition. among 1,565 TIA/stroke survivors with 194 hospital admissions (158 patients, mean/standard deviation age at admission = 79.2/11.5 years), delirium occurred in 59 (37%). WMC and atrophy on baseline imaging were associated with delirium [odds ratio (OR) = 3.41, 1.21–5.85, P = 0.001 and OR = 2.50, 1.23–5.08, P = 0.01 (unadjusted) and OR = 2.67, 1.21–5.85, P = 0.02 and OR = 2.18, 1.00–4.73, P = 0.05 (adjusted age and sex)]. Associations were strengthened when analyses were restricted to patients hospitalised within 5 years of baseline brain imaging [OR = 6.04, 2.39–15.24, P < 0.0001 and OR = 4.64, 1.46–14.82, P = 0.009 (unadjusted)] but only WMC remained significant after adjustment for all covariates including pre-admission cognition (OR = 4.83, 1.29–18.13, P = 0.02 for Mini-Mental State Examination and OR = 5.15, 1.26–21.09, P = 0.02 for Montreal Cognitive Assessment). WMC and atrophy on brain imaging done up to 5 years earlier predicted delirium and may have clinical utility in risk stratification. Associations with WMC but not atrophy were independent of pre-admission cognitive impairment.

Background and Purpose: The PROGRESS trial (Perindopril Protection Against Recurrent Stroke Study) conducted in the early 1990s showed that blood pressure (BP) lowering therapy reduced the risks of recurrent stroke by about 50% after spontaneous intracerebral hemorrhage (ICH). However, the ICH subgroup was a minority, and trial cohorts are invariably selective. Therefore, it is unclear whether the impact of BP control on risk of recurrent stroke in ICH observed in PROGRESS would be as great in real-world practice. Methods: We compared BP control (mean BP during study follow-up) and risks of recurrent stroke after first-ever primary ICH in 2 colocated population-based studies before and after the PROGRESS trial (1995–2001) in Oxfordshire: Oxfordshire Community Stroke Project (OCSP; 1981–1986) and OXVASC (Oxford Vascular Study; 2002–2018). Results: Two hundred seventy-seven patients (753 patient-years of follow-up) with first-ever primary ICH were ascertained in OXVASC and OCSP. Baseline systolic BP was comparable between the 2 studies (mean/SD=183.8/36.5 in OXVASC versus 178.1/38.2 in OCSP, P =0.30) but among one hundred thirty-seven 90-day survivors, mean BP during follow-up was substantially lower in OXVASC versus OCSP (135.2/16.4 versus 157.3/17.8, P P =0.006), predominantly driven by a reduction at younger ages (5-year risk at age P =0.001; hazard ratio, 0.14 [0.04–0.54]). Conclusions: Risks of recurrent stroke after primary ICH have fallen significantly in Oxfordshire over the past 4 decades, coinciding with substantial improvements in BP control during follow-up.

Introduction Unruptured intracranial aneurysms (UIAs) are common incidental imaging findings, but there are few data in patients with transient ischaemic attack (TIA)/stroke. The frequency of UIA might be higher due to shared risk factors, but rupture risk might be reduced by intensive secondary prevention. We determined the prevalence and prognosis of UIA in patients with suspected TIA/minor stroke. Methods All patients referred to the population-based Oxford Vascular Study (2011–2020) with suspected TIA/minor stroke and non-invasive angiography were included. We determined the prevalence of incidental asymptomatic UIA and the risk of subsequent subarachnoid haemorrhage (SAH) by follow-up on intensive medical treatment, with guideline-based monitoring/management. We also did a systematic review of UIA prevalence/prognosis in cohorts with TIA/stroke. Findings Among 2013 eligible patients, 95 (4.7%) had 103 previously unknown asymptomatic UIA. Female sex (OR 2.3, 95% CI 1.5 to 3.7), smoking (2.1, 1.2 to 3.6) and hypertension (1.6, 1.0 to 2.5) were independently predictive of UIA, with a prevalence of 11.1% in those with all three risk factors. During mean follow-up of 4.5 years, only one SAH occurred: 2.3 (95% CI 0.3 to 16.6) per 1000 person-years. We identified 19 studies of UIA in TIA/stroke cohorts (n=12 781), all with either symptomatic carotid stenosis or major acute stroke. The pooled mean UIA prevalence in patients with TIA/stroke was 5.1% (95% CI 4.8 to 5.5) and the incidence of SAH was 4.6 (95% CI 1.9 to 11.0) per 1000 person-years. Interpretation The 5% prevalence of UIA in patients with confirmed TIA/minor stroke is likely higher than that in the general population. However, the risk of SAH on intensive medical treatment and guideline-based management/monitoring is low.

Background While anatomic features associated with the risk of posterior communicating artery (PcoA) occlusion after embolization of aneurysms of the PcoA segment of the internal carotid artery (ICA) are well known, the link between perforator origin and perforator infarction has only been reported following neurosurgical clipping. The aim of this study was to determine the origin of anterior thalamic perforators and correlate it with risk of perforator infarction after embolization of PcoA segment aneurysms. Methods One-hundred-and-ninety consecutive patients treated for PcoA segment aneurysms between 2017 and 2019 were included. PcoA and anterior thalamic perforator origin anatomy was assessed with computed tomography (CT) angiography, digital subtracted angiography, and high-resolution three-dimensional rotational cone-beam CT angiography (CBCT-A) by two independent interventional neuroradiologists. The presence of perforator infarction after embolization was ascertained from the patient’s notes and follow-up imaging. Results CBCT-A was superior in demonstrating the origin of perforators (PConclusions Our study suggests that anterior thalamic perforators may arise from aneurysm wall when there is no PcoA. Anatomic association between PcoA agenesis and perforator arising from ICA could underlie such findings, and careful consideration is essential before aneurysm repair to anticipate the risk of thalamic infarction in such cases.