Atherosclerotic disease of the carotid arteries is a crucial risk factor in predicting the likelihood of future stroke events. In addition, emerging studies suggest that carotid stenosis may also be an indicator of plaque load on coronary arteries and thus have a correlation with the risk of acute cardiovascular events. Furthermore, although in symptomatic patients the degree of stenosis is the main morphological parameter studied, recent evidence suggests, especially in asymptomatic patients, that plaque vulnerability should also be evaluated as an emerging and significant imaging parameter. The reference diagnostic methods for the evaluation of carotid stenosis are currently ultrasonography, magnetic resonance imaging (MRI), and computed tomography angiography (CTA). In addition, other more invasive methods such as 123I-metaiodobenzylguanidine (MIBG) scintigraphy and PET-CT, as well as digital subtraction angiography, can be used. Each method has advantages and disadvantages, and there is often some confusion in their use. For example, the usefulness of MRI is often underestimated. In addition, implementations for each method have been developed over the years and are already enabling a significant increase in diagnostic accuracy. The purpose of our study is to make an in-depth analysis of all the methods in use and in particular their role in the diagnostic procedure of carotid stenosis, also discussing new technologies.

At the time of diagnosis, the vast majority of prostate carcinoma patients have a clinically localized form of the disease, with most of them presenting with low- or intermediate-risk prostate cancer. In this setting, various curative-intent alternatives are available, including surgery, external beam radiotherapy and brachytherapy. Randomized clinical trials have demonstrated that moderate hypofractionated radiotherapy can be considered as a valid alternative strategy for localized prostate cancer. High-dose-rate brachytherapy can be administered according to different schedules. Proton beam radiotherapy represents a promising strategy, but further studies are needed to make it more affordable and accessible. At the moment, new technologies such as MRI-guided radiotherapy remain in early stages, but their potential abilities are very promising.

Background/Objectives: The Mediator (MED) complex is an essential regulator of RNA polymerase II transcription. There is increasing evidence that pathogenic variants in several MED subunits are the cause of neurodegenerative and neurodevelopmental phenotypes, collectively referred to as “MEDopathies”. This review aims to summarize current knowledge on the genetic basis, clinical manifestations, and neuroradiological features of MED-related disorders. Methods: We undertook a narrative synthesis of the literature focusing on the MED subunits most commonly associated with neurological disorders, including MED1, MED8, MED11, MED12/MED12L, MED13/MED13L, MED14, MED17, MED20, MED23, MED25, MED27, and CDK8. Sources included peer-reviewed genetic, clinical, and imaging studies, supplemented by relevant case reports and cohort analyses. In addition, representative facial phenotypes associated with selected MED variants (MED11, MED12, MED13, MED13L, MED25) were visualized for educational purposes using artificial intelligence-based image generation derived from standardized clinical descriptors. Results: All MEDopathies show converging clinical patterns: global developmental delay/intellectual disability, hypotonia, epilepsy, speech disorders, and behavioral comorbidity. Non-neurological involvement, such as craniofacial or cardiac anomalies, is subunit-specific. Neuroradiological features include callosal abnormalities (agenesis, thinning, dysmorphia), delayed or hypomyelination, progressive cerebral and cerebellar atrophy, basal ganglia signaling changes, pontine hypoplasia, and, in MED27 deficiency, a “hot cross bun” sign. Gene-specific constellations emphasize catastrophic infantile progression (MED11), X-linked syndromes with callosal defects (MED12/MED12L), language-dominant phenotypes (MED13), and syndromic intellectual disability with systemic features (MED13L). Conclusions: The growing spectrum of MEDopathies argues for their recognition as a unified nosological group with overlapping clinical and radiological signatures. Characteristic MRI constellations may serve as diagnostic clues and guide targeted molecular testing. Future directions include longitudinal imaging to describe disease progression and the integration of genomic data with curated clinical radiological datasets to refine genotype-phenotype correlations.

Background: Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) is an uncommon inflammatory disorder of the central nervous system that is exceptionally rare during childhood. Although pontocerebellar punctate enhancement is considered its neuroradiological hallmark, the full spectrum of pediatric clinical and imaging manifestations remain poorly characterized because available evidence is limited to isolated case reports and small case series. We conducted a systematic review to characterize the clinical presentation, neuroimaging phenotype, diagnostic challenges, therapeutic strategies, and outcomes of pediatric CLIPPERS. Methods: A systematic literature search was conducted in PubMed/MEDLINE and Scopus from database inception to December 2025, following PRISMA guidelines. Studies reporting patients younger than 18 years with a diagnosis of CLIPPERS were eligible. Clinical, neuroradiological, laboratory, histopathological, therapeutic, and outcome data were extracted using a standardized form. Diagnostic certainty was assessed according to the Tobin criteria, and methodological quality was evaluated using the Joanna Briggs Institute (JBI) critical appraisal tools. Results: Ten studies comprising 13 pediatric patients fulfilled the inclusion criteria. Median age at presentation was 13 years (range 3–16 years), with a slight male predominance. Ataxia was the most common presenting manifestation (84.6%), followed by cranial nerve involvement (61.5%) and diplopia (46.2%). Magnetic Resonance Imaging (MRI) consistently demonstrated brainstem involvement, predominantly affecting the pons (84.6%) and cerebellum (76.9%), while supratentorial lesions (46.2%), midbrain involvement (46.2%), and spinal cord abnormalities (23.1%) suggest that the neuroradiological phenotype may extend beyond the classic pontocerebellar pattern, although these findings were observed in a limited number of patients. Cerebrospinal fluid (CSF) findings were nonspecific, typically showing normal results or mild lymphocytic pleocytosis. Histopathological examination, when available, demonstrated characteristic perivascular T-cell-predominant inflammatory infiltrates. All patients received high-dose corticosteroids with initial clinical improvement; however, relapses occurred in 61.5% of cases, frequently during corticosteroid tapering, often requiring steroid-sparing immunosuppressive therapy. Based on the available evidence, we suggest a practical clinic-radiological framework to facilitate the evaluation of children presenting with suspected CLIPPERS. Conclusions: Pediatric CLIPPERS represents a rare but increasingly recognized neuroinflammatory disorder characterized by marked corticosteroid responsiveness and a wide range of neuroradiological phenotypes. Although pontocerebellar involvement remains the defining imaging feature, supratentorial and spinal cord lesions are not uncommon and should not exclude the diagnosis after careful consideration of alternative inflammatory, autoimmune, infectious, and neoplastic disorders. Given the high relapse rate and the limited quality of available evidence, prolonged follow-up and collaborative multicenter studies are needed to refine pediatric diagnostic criteria and optimize long-term management.