Purpose To report the results of a retrospective analysis of prospectively collected data evaluating the safety and efficacy of a double layer stent engineered for carotid artery occlusive disease. Methods Between January 2014 and February 2017, 138 patients (25.4% women; median age 71 years) underwent Casper stent implantation for carotid artery stenosis. Eligibility criteria included stenosis >70% of vessel diameter (or >50% diameter with ulceration) in symptomatic patients or asymptomatic patients with >80% stenosis at the carotid bifurcation or in the proximal internal carotid artery. For all procedures, a distal embolic protection device was used. The primary endpoint was the rate of 90 day major adverse neurological events, defined as minor stroke, major stroke, or death by independent neurological assessment. Results Stent deployment was completed successfully in all cases without documented technical failure. There were no adverse neurological events or mortalities within 90 days. One thromboembolic occlusion of a small distal branch of the anterior cerebral artery occurred during the procedure and resolved with systemic recombinant tissue plasminogen activator administration. New ischemic lesions, all clinically silent, were seen in 6.5% of patients on post-procedure cerebral MRI. Conclusion The Casper carotid stent demonstrated safety and efficacy in the treatment of carotid stenosis, with no technical failures and no adverse neurological events seen throughout the 90 day follow-up period. Its double layer structure seems to combine adequate plaque scaffolding with high vessel adaptability.

Objective: Status epilepticus (SE) is frequently associated with peri‐ictal magnetic resonance imaging (MRI) abnormalities (PMA). However, the anatomical distribution of these alterations has not been systematically studied. The aim of this study was to assess the localization patterns of PMA in patients with SE. Methods: In this prospective case–control study, we compared the distribution and combinations of diffusion‐restricted PMA to diffusion‐restricted lesions caused by other neurological conditions. All patients of the SE group and the control group underwent MRI including a diffusion‐weighted imaging sequence. Patients with SE were imaged within 48 h after its onset. Results: We enrolled 201 patients (51 with SE and 150 controls). The most frequent locations of PMA in SE were cortex (25/51, 49%), followed by hippocampus (20/51, 39%) and pulvinar of thalamus (10/51, 20%). In the control group, the cortex was involved in 80 of 150 (53%), white matter in 53 of 150 (35%), and basal ganglia in 33 of 150 (22%). In the control group, the pulvinar of thalamus was never affected and hippocampal structures were rarely involved (7/150, 5%). Involvement of the pulvinar of thalamus and the hippocampus had high specificity for SE at 100% (95% confidence interval [CI] = 98–100) and 95% (95% CI = 91–98), respectively. The sensitivity, however, was low for both locations (pulvinar of thalamus: 20%, 95% CI = 10–33; hippocampus: 39%, 95% CI = 26–54). Significance: Diffusion‐restricted MRI lesions observed in the pulvinar of thalamus and hippocampus are strongly associated with SE. These changes may help physicians in diagnosing SE‐related changes on MRI in an acute setting, especially in cases of equivocal clinical and electroencephalographic manifestations of SE.

Background: The pathological mechanism in acute spinal cord injury (SCI) is dual sequential: the primary mechanical lesion and the secondary injury due to a cascade of biochemical and pathological changes initiated by the primary lesion. Therapeutic approaches have focused on modulating the mechanisms of secondary injury. Despite extensive efforts in the treatment of SCI, there is yet no causal, curative treatment approach available. Extracorporeal shock wave therapy (ESWT) has been successfully implemented in clinical use. Biological responses to therapeutic shock waves include altered metabolic activity of various cell types due to direct and indirect mechanotransduction leading to improved migration, proliferation, chemotaxis, modulation of the inflammatory response, angiogenesis, and neovascularization, thus inducing rather a regeneration than repair. The aim of this clinical study is to investigate the effect of ESWT in humans within the first 48 h after an acute traumatic SCI, with the objective to intervene in the secondary injury phase in order to reduce the extent of neuronal loss. Methods: This two-arm three-stage adaptive, prospective, multi-center, randomized, blinded, placebo-controlled study has been initiated in July 2020, and a total of 82 patients with acute traumatic SCI will be recruited for the first stage in 15 participating hospitals as part of a two-armed three-stage adaptive trial design. The focused ESWT (energy flux density: 0.1–0.19 mJ/mm², frequency: 2–5 Hz) is applied once at the level of the lesion, five segments above/below, and on the plantar surface of both feet within the first 48 h after trauma. The degree of improvement in motor and sensory function after 6 months post-injury is the primary endpoint of the study. Secondary endpoints include routine blood chemistry parameters, the degree of spasticity, the ability to walk, urological function, quality of life, and the independence in everyday life. Discussion: The application of ESWT activates the nervous tissue regeneration involving a multitude of various biochemical and cellular events and leads to a decreased neuronal loss. ESWT might contribute to an improvement in the treatment of acute traumatic SCI in future clinical use. Trial registration: ClinicalTrials.gov NCT04474106

Objective: To assess and compare the detection rates of peri‐ictal abnormalities using magnetic resonance imaging (MRI) and computed tomography perfusion (CTP) in patients with non‐convulsive status epilepticus (NCSE). Methods: We conducted a systematic literature search in five databases up to February 2025. Studies reporting peri‐ictal MRI abnormalities (PMAs) or cerebral perfusion abnormalities (CPAs) in patients with NCSE were included. Meta‐analyses of proportions were performed using a random‐effects model. Subgroup analyses and meta‐regression were used to compare detection rates across imaging modalities. Results: Nineteen studies were included (15 MRI, 4 CTP), comprising 562 patients for MRI and 72 for CTP. The pooled detection rate of peri‐ictal abnormalities was 50.0% (95% confidence interval [CI]: 34.0%–65.0%) for MRI and 79.3% (95% CI: 54.3%–92.5%) for CTP. Among the MRI modalities, arterial spin labeling (ASL) demonstrated the highest detection rate at 88.8% (95% CI: 32.9%–99.2%). CTP showed a significantly higher detection rate than MRI ( χ ² = 3.97, p = 0.046); meta‐regression indicated increased odds of detection with CTP (odds ratio [OR] = 4.06, 95% CI: 0.97–16.99, p = 0.055). No statistically significant difference was found between ASL and CTP ( χ ² = 0.22, p = 0.636). Conclusions: CTP demonstrates a higher detection rate than conventional MRI for peri‐ictal abnormalities in patients with NCSE, supporting its utility in rapid diagnosis and differential workup. Among MRI sequences, ASL showed the highest detection rates, highlighting its potential role in the diagnostic assessment of NCSE. Although MRI remains essential for clarifying etiology, its effectiveness in detecting PMA is highly dependent on the sequences used.

Here, we report on a 28-year old male patient presenting with neck and shoulder pain, dysesthesia of all four limbs and hypesthesia of both hands, without motor deficits. Magnetic resonance imaging showed an intradural, intramedullary mass of the cervical spinal cord of 6.4 cm length and 1.7 cm diameter. The patient underwent surgical resection. Histological and immunohistochemical evaluation showed pleomorphic glial tumor cells, mitoses, calcifications, and atypical ganglioid cells compatible with the morphology of anaplastic ganglioglioma (WHO Grade III). Extensive molecular workup revealed H3F3A K27M, TERT C228T and PDGFRα Y849C mutations indicating poor prognosis. The H3F3A K27M mutation assigned the tumor to the molecular group of diffuse midline glioma (WHO Grade IV). Epigenome-wide methylation profiling confirmed the methylation class of diffuse midline glioma. Thus, this is a very rare case of malignant glioma with H3 K27M genotype phenotypically mimicking anaplastic ganglioglioma. This case emphasizes the importance of comprehensive morphological and molecular workup including methylome profiling for advanced patient care.