Background: Bone or cartilage anomalies with affection of brain supplying arteries are a potential structural cause for ischemic stroke. In the following, we termed this entity bony stroke. Due to rarity of their description, there is no standardized workup and therapy for bony strokes. Methods: Retrospectively, we extracted diagnostic and therapeutic workup of all patients considered to have had a bony stroke between January 2017 to March 2022 at our comprehensive care center. Results: In total, 6 patients classified as a bony stroke were identified among 4200 acute patients with ischemic stroke treated during the study period. Each patient had recurrent ischemic strokes in the dependent vascular territory before diagnosis. Diagnosis was achieved by a combination of imaging devices, including sonography, computed tomography, and magnetic resonance imaging. In addition to conventional static imaging, the application of dynamic imaging modalities with the patients’ head in rotation or reclination confirmed a vessel affection following head movements in 3 patients (50%). Treatment options were interdisciplinary assessed and included the following: conservative treatment (n=1), endovascular stenting (n=2) or occlusion (n=2), surgical removal of bone/ cartilage (n=2), and surgical bypass treatment (n=1). In follow-up (mean 11.7 months), no patient experienced further ischemia. Conclusions: As a differential diagnosis, bony strokes may be considered in patients with recurrent ischemic stroke of unknown cause in one dependent vascular territory. Interdisciplinary evaluation and treatment may eliminate risk of stroke recurrence.

We present an 81-year old male in whom a routine carotid artery ultrasonographic follow-up examination incidentally revealed a large, free-floating thrombus (FFT) of the right internal carotid artery. This case focuses on the clinical decision-making regarding FFTs, which constitute a rare condition lacking a diagnostic gold standard with few available data concerning optimum treatment and natural course-in particular regarding patients in whom FFT is an incidental finding. We were able to demonstrate the accuracy of carotid artery ultrasonography in the detection as well as follow-up of FFT. Of clinical interest is furtherly a possible partial disappearance by spontaneous re-adhesion or resolution of the FFT.

Although a pathophysiological impact remains difficult to prove in individual patient care, a patent foramen ovale (PFO) is currently considered of high relevance for secondary prophylaxis in selected patients with cryptogenic ischemic stroke. By quantification of histological clot composition, we aimed to enhance pathophysiological understanding of PFO attributable ischemic strokes. Retrospectively, we evaluated all cerebral clots retrieved by mechanical thrombectomy for acute ischemic stroke treatment between 2011 and 2021 at our comprehensive stroke care center. Inclusion criteria applied were cryptogenic stroke, age (≤60 years), and PFO status according to transesophageal echocardiography, resulting in a study population of 58 patients. Relative clot composition was calculated using orbit image analysis to define the ratio of main histologic components (fibrin/platelets (F/P), red blood cell count (RBC), leukocytes). Cryptogenic stroke patients with PFO (PFO+, n = 20) displayed a significantly higher percentage of RBC (0.57 ± 0.17; p = 0.002) and lower percentage of F/P (0.38 ± 0.15; p = 0.003) compared to patients without PFO (PFO–, n = 38) (RBC: 0.41 ± 0.21; F/P: 0.52 ± 0.20). In conclusion, histologic clot composition in cryptogenic stroke varies depending on the presence of a PFO. Our findings histologically support the concept that a PFO may be of pathophysiological relevance in cryptogenic ischemic stroke.

Visit-to-visit heart rate variation (HRV-VV) is associated with mortality and cardiovascular events. Mechanisms of the interaction between HRV-VV and vascular disease are not clearly understood. Our study aimed to evaluate the association between HRV-VV and carotid intima-media thickness (IMT) and their potential impact on cardiovascular disease development. The study population is derived from a cohort of elderly patients enrolled in the primary-care-based INtervention project on cerebroVAscular diseases and Dementia in the community of Ebersberg (INVADE). We included all patients with a follow-up of eight years and five follow-up visits in regular two-year intervals. HRV-VV was defined by the standard deviation of between-visit measurements (SD). Uni- and multivariable regression models were used to identify associations between HRV-VV, IMT, and a combined cardiovascular endpoint of new onset stroke and myocardial infarction. 2815 patients were included in the study. HRV-VV was positively associated with IMT in multivariable analysis (p = 0.026). Every SD HRV-VV of 10 bpm was associated with a change of IMT of 18 ± 8 µm. Furthermore, HRV-VV showed a numerical and positive association with the combined cardiovascular endpoint (p = 0.07), while a simultaneous increase in HRV-VV and IMT increased the likelihood more than either factor alone (p = 0.009). HRV-VV showed a positive association with IMT, a surrogate marker for early arteriopathy. Both parameters furtherly demonstrated a synergistic impact on the likelihood of cardiovascular disease development. Given its widespread availability by continuous monitoring with wearables, HRV-VV may provide a potentially modifiable medical target for personalized cardiovascular risk stratification.

Background: Although large-vessel vasculitis (LVV) can affect both the anterior and posterior intracranial circulation, routine neurosonographic follow-up, including transcranial duplex sonography, has not been established. We aimed to characterize patients with giant cell arteritis (GCA) and Takayasu arteritis (TAK) regarding the detection of progressive or new-onset inflammatory vessel changes by using neurosonography, and to assess the impact on medical or interventional treatment strategies. Methods: We retrospectively identified all patients with LVV treated at our neurological department between January 2015 and October 2025 with at least one neurosonographic follow-up examination. Baseline and follow-up sonographic data, clinical characteristics, medical therapy, and interventional treatments were analyzed. Results: In total, 21 LVV patients (GCA, n = 16; TAK, n = 5) underwent sonographic follow-up (GCA: median 28 (2–106) months, 4.5 (2–33) sonographic assessments; TAK: 75 (33–255) months, 14 (4–60) sonographic assessments). Isolated or combined, progressive or new-onset intra- and extracranial arterial disease was detected in seven of the 16 GCA patients (43.8%), of whom three (18.8%) presented with ischemic stroke. Medical treatment was adapted in four progressive cases. In two patients, additional interventional treatment was performed. Among TAK, two of five (40%) patients showed progressive sonographic changes, with one patient experiencing an ischemic stroke requiring endovascular treatment for progressive common carotid artery stenosis and one patient showing asymptomatic intracranial ICA involvement. Conclusions: Progressive and symptomatic involvement of intracranial carotid and vertebral arteries is a frequent finding in patients with LVV. These changes can be effectively detected through comprehensive neurosonographic follow-up, including transcranial ultrasound assessment.