Purpose: Myocardial injury, indicated by an elevation of high-sensitive cardiac Troponin (hs-cTnT), is a frequent stroke-related complication. Most studies investigated patients with ischemic stroke, but only little is known about its occurrence in patients with intracerebral hemorrhage (ICH). This study aimed to assess the frequency, predictors, and implications of myocardial injury in ICH patients. Methods: Our retrospective analysis included 322 ICH patients. We defined myocardial injury as an elevation of hs-cTnT above the 99th percentile (i.e. 14 ng/L). Acute myocardial injury was defined as either a changing pattern of > 50% within 24 h or an excessive elevation of initial hs-cTnT (> 52 ng/L). 3D brain scans were assessed for ICH visually and quantitatively by a deep learning algorithm. Multiple regression models and Voxel-based Lesion-Symptom Mapping (VLSM) were applied. Results: 63.0% (203/322) of patients presented with myocardial injury, which was associated with more severe strokes and worse outcomes during the in-hospital phase (P < 0.01). Acute myocardial injury occurred in 24.5% (79/322) of patients. The only imaging finding associated with acute myocardial injury was midline shift (69.8% vs. 44.6% for normal or stable hs-cTnT, P < 0.01), which also independently predicted it (odds ratio 3.29, confidence interval 1.38–7.87, P < 0.01). In contrast, VLSM did not identify any specific brain region significantly associated with acute myocardial injury. Acute myocardial injury did not correlate with preexisting cardiac diseases; however, the frequency of adverse cardiac events was higher in the acute myocardial injury group (11.4% vs. 4.1% in patients with normal and/or stable patterns of hs-cTnT, P < 0.05). Conclusion: Myocardial injury occurs frequently in ICH and is linked to poor outcomes. Acute myocardial injury primarily correlates to space-occupying effects of ICH but is less dependent on premorbid cardiac status. Nonetheless, it is associated with a higher rate of adverse cardiac events.

Background: In addition to infectious fever, stroke-related disturbances in thermoregulation, referred to as central fever, are frequently observed in patients with stroke, particularly in those with intracerebral haemorrhage (ICH). Rapid identification of the underlying cause of fever is crucial for treatment decisions. This study aims to identify clinical, laboratory and radiological parameters that differentiate central fever from infectious fever in patients with ICH. Methods: We included 547 ICH patients in this retrospective, single-centre cohort study. Fever was defined as a body temperature exceeding 38.3°C for at least 2 consecutive days. Central fever was characterised by the absence of an infection diagnosis, cultured pathogens and any other identified cause of fever. CT scans were assessed visually and with a 3D nn-UNet for segmentation and subsequent quantification of all ICH components. Voxel-based lesion-symptom mapping was performed to identify lesion locations related to central fever. Univariate analyses and multiple logistic regression were conducted. Results: Fever occurred in 213 patients: 54 with central fever, 156 with infectious fever and 3 with other causes. Central fever was linked to higher scores on the National Institutes of Health Stroke Scale and worse outcomes (p<0.01). It had an earlier onset (median day 2 (1–3) vs 6 (4–9) p<0.01) and was more frequent in patients with lesions affecting the left midbrain and hypothalamic region (p<0.01). In contrast, infectious fever was associated with higher levels of infectious parameters (ie, C reactive protein, procalcitonin and leucocyte count). Its early onset (p<0.001) and affection of the left hypothalamic region (OR=9.7 (1.6 to 58.837), p=0.013) emerged as independent predictors of central fever. Conclusions: Early onset and hypothalamic involvement are the strongest indicators of central fever, which may help guide evidence-based treatment decisions for patients with fever following ICH.

Background and Purpose: Decompressive surgery is a potentially life-saving treatment in patients with malignant space-occupying cerebellar infarction. However, there is only limited literature on functional outcomes and complications after surgery. Our aim was to establish markers which predict poor outcome. Methods: We retrospectively analyzed data of all patients who underwent surgery due to malignant swelling of a space-occupying cerebellar infarction in our hospital between 2005 and 2023. Statistical analyses were conducted on multiple parameters to identify predictors of poor functional outcome (mRS 4–6) 90 days after surgery. Complications during hospitalization were reviewed for each patient. Results: In total, 58 patients received decompressive surgery. The 90-day mortality rate was 27.6% (n = 16). A good functional outcome (mRS 0–3) 90 days after surgery was achieved in 24 patients (41.4%). Multivariable analysis revealed multiple factors associated with a poor outcome on day 90 (mRS 4–6): a higher premorbid mRS score (OR 2.715 [95% CI, 1.166–6.323]; p = 0.021), higher NIHSS score on admission (OR 1.088 [95% CI, 1.014, 1.168]; p = 0.019) and the presence of an additional brainstem infarction (OR 7.035, [95% CI, 1.255, 39.424], p = 0.027). Hyperactive delirium was associated with good clinical outcome (OR 0.020 [95%CI, 0.001–0.623]; p = 0.026). Aspiration pneumonia (n = 22, 37.9%), urinary tract infection (n = 15, 25.9%), and hyperactive delirium (n = 8, 13.8%) were the most common complications during hospitalization. Conclusions: Decompressive surgery is a safe, life-saving treatment for malignant space-occupying cerebellar infarction. Higher premorbid mRS, higher NIHSS score on admission and the presence of brainstem infarction are associated with a poor functional outcome.

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.