Cerebral Palsy (CP) is a neurodevelopment disorder caused by improper brain development or harm to the developing brain and is the underlying cause of the most common motor disability in children. The clinical symptoms vary between subjects because the etiology is complex and can affect a variety of anatomical structures and each of these can lead to a different symptom. The motor dysfunction is often associated with sensory, perceptual, cognitive, communication and behaviour impairments as well as epilepsy and secondary musculoskeletal disorders which have a significant influence on the child’s quality of life, activity, and participation. The risk of developing CP is present in infants born preterm, but these children sum up less than 50% of cases. The factors that cause CP in children born at term are grouped in antenatal, perinatal, neonatal, some of them can be modified like alcohol consumption, maternal smoking, infections, but others like genetic factor cannot be modified. CP can be classified in different ways depending on the clinical manifestation. Throughout time classification was based on the type and distribution of motor anomalies, which often corresponded to the area of injury. Spastic subtypes, dyskinetic subtypes, and ataxic subtypes are the three basic forms of motor dysfunction. The most common conditions associated with CP are pain, intellectual disability, speech disorder, bladder control problems, epilepsy, and behaviour disorders. Early intervention is thought to be the most effective treatment for CP. As soon as the diagnosis is determined, rehabilitation treatment should begin. The earlier a rehabilitation intervention begins, the better the prospects of improving the child’s functional abilities and independence.

Stroke is the second leading cause of death worldwide. The global incidence of stroke has increased in recent years, although low and middle-income countries have been heavily affected. Because of the complicated and diversified physical and emotional disruption, stroke survivors are likely to face a variety of difficulties in daily life activities. Because of the wide impact of a stroke on all body structures and functions, there is no gold standard instrument to evaluate impairment and all elements of recovery after a stroke, and there is no single scale that can capture all the effects of a stroke. The International Classification of Impairments, Disability, and Handicaps (ICIDH) categorized the consequences of the diseases into three categories: impairment, disability, and handicap. Using the biopsychosocial model in 2001 WHO defines and classifies disability by using International Classification of Functioning Disability and Health (ICF). The ICF divides the impairment into three categories: body function and structure, activity, and participation. This article aims to review the most important tools that are reliable and valid in assessing the disability left after a stroke: The National Institute of Health Stroke Scale (NIHSS), Barthel index (BI), The modified Rankin scale (mRS), Instrumental activities of daily living (IADL), Glasgow outcome scale (GOS), The Functional Independence Measure (FIM), The World Health Organization Disability Assessment Schedule (WHODAS 2.0). The WHODAS 2.0 questionnaire is validated in several countries and it would be useful to be validated, also, in our country.

Background and Objectives: Acute and obstructive pyelonephritis (AOP) management, despite advancements in diagnostic imaging and antimicrobial therapy, is characterized by delayed recognition and increasing antimicrobial resistance. This review aimed to summarize current evidence regarding the clinical characteristics, microbiological spectrum, biomarkers, and imaging findings associated with AOP. Materials and Methods: A systematic review was conducted according to PRISMA guidelines and registered in PROSPERO (CRD420251162736). Literature searches were performed across the PubMed, Scopus, and Web of Science databases for articles published between January 2014 and 31 March 2025 using the term “acute obstructive pyelonephritis”. Inclusion criteria comprised original full-text English-language studies, published in the last 10 years and conducted in adults, reporting clinical, laboratory, microbiological, and imaging characteristics. Exclusion criteria are letters to the editor, expert opinions, case reports, conference or meeting abstracts, reviews, and redundant publications; having unclear or incomplete data; and being performed on cell cultures or on mammals. The quality of included studies was assessed using the Newcastle–Ottawa Scale. Results: Twenty-three studies met the inclusion criteria. AOP predominantly affected elderly patients with comorbidities, especially diabetes mellitus and urinary tract obstruction. Predictors of septic shock included thrombocytopenia, hypoalbuminemia, elevated procalcitonin (>1.12 µg/L), presepsin, and a neutrophil-to-lymphocyte ratio ≥ 8.7. Escherichia coli remained the leading pathogen (60–95%) with extended-spectrum β-lactamase (ESBL) rates between 20 and 70%, followed by Klebsiella pneumoniae. CT demonstrated 71–100% sensitivity for detecting obstructive complications, confirming its superiority over ultrasound, while MRI provided comparable diagnostic accuracy in selected cases. Source control through double-J stenting or percutaneous drainage significantly improved survival. Conclusions: AOP requires prompt recognition and early decompression to prevent sepsis-related mortality. Biomarkers such as procalcitonin, presepsin, and neutrophil to lymphocyte ratio enhance risk stratification, while CT remains the gold-standard imaging modality. The increasing prevalence of ESBL-producing pathogens underscores the need for antimicrobial stewardship and individualized therapeutic strategies guided by local resistance data.

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is highly prevalent in patients with type 2 diabetes (T2D) and is associated with increased cardiovascular risk. However, the relative contribution of traditional cardiometabolic risk factors (CMRFs), hepatic fibrosis markers, and antidiabetic therapies to atherosclerosis remains unclear. Methods: We conducted a cross-sectional study including 46 patients with T2D and MASLD. Atherosclerotic cardiovascular disease (ASCVD) was defined as the presence of carotid atheromatosis, stroke, peripheral arterial disease, or ischemic heart disease, as assessed by imaging-based parameters. Clinical, metabolic, and treatment-related variables were analyzed, including age, Hemoglobin A1c (HbA1c), lipid profile, hepatic fibrosis indices such as Fibrosis-4 index (FIB-4), and antidiabetic therapies (sodium–glucose cotransporter-2 inhibitors (SGLT2is), glucagon-like peptide-1 receptor agonists (GLP-1 RAs), and insulin). Multivariable regression models and receiver operating characteristic (ROC) curve analyses were used to evaluate associations and discriminative performance. Results: Traditional CMRFs were more strongly associated with ASCVD than hepatic fibrosis markers or antidiabetic therapies. Age was associated with ASCVD in several exploratory models, although this association was attenuated in the fully adjusted model. HbA1c showed the highest discriminative performance (AUC 0.77), indicating that chronic glycemic exposure is a major determinant of vascular disease in this cohort. In contrast, FIB-4 was not associated with ASCVD and did not improve model performance. Antidiabetic therapies, including SGLT2i and GLP-1 RAs, were not independently associated with ASCVD. Insulin therapy was more frequent among patients with ASCVD, but was not independently associated after adjustment. Conclusions: In patients with T2D and MASLD, ASCVD appears to be associated with traditional CMRFs, particularly chronic glycemic exposure, rather than hepatic fibrosis markers or treatment status. These findings highlight the central role of metabolic control in cardiovascular risk and suggest that the contribution of liver-related markers and therapeutic interventions may be more relevant in longitudinal settings.

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is highly prevalent among patients with type 2 diabetes (T2D) and has been increasingly recognized as a potential contributor to cardiovascular (CV) disease. However, the relationship between MASLD and subclinical/clinical atherosclerosis remains controversial, with inconsistent findings across imaging modalities and study populations. Methods: A systematic review was conducted according to PRISMA guidelines and registered in PROSPERO (CRD420261347480). Literature searches were performed across the PubMed, Scopus, and Web of Science library databases from 1 January 2016 to 27 March 2026, using the terms: “MASLD AND (type 2 diabetes OR type 2 diabetes mellitus OR T2DM) AND atherosclerotic plaque” for each of the three databases. Inclusion criteria comprised original full-text English-language studies, published in the last 10 years and conducted in adults, reporting data regarding the evaluation of atherosclerosis in patients with T2D and MASLD/NAFLD. Exclusion criteria are letters to the editor, expert opinions, case reports, conference or meeting abstracts, reviews, and redundant publications; having unclear or incomplete data; and being performed in vitro (cell cultures) or in animal models. The quality of included studies was assessed using the Newcastle–Ottawa Scale. Results: The included studies, predominantly cross-sectional and a single longitudinal study, as well as different modalities of evaluating atherosclerosis, showed heterogeneous findings. MASLD is associated with increased carotid plaque progression, including in lean individuals. Its relationship with carotid intima-media thickness (CIMT) is inconsistent across studies, with some reporting higher values and others finding no significant association after adjustment. Hepatic fibrosis appears more strongly linked to vascular aging than steatosis alone, with variability likely due to differences in study methods and populations. Conclusions: The presence of both MASLD and T2D may be associated with atherosclerosis across different stages, from subclinical changes to clinically manifest disease, particularly at more advanced stages such as plaque presence or progression, whereas its relationship with early markers like pulse wave velocity or CIMT remains inconsistent. Liver fibrosis may represent a stronger determinant of atherosclerosis than hepatic steatosis alone. Although the evidence base is limited and largely derived from a small number of predominantly cross-sectional studies, further standardized and prospective research is warranted to better define these relationships and evaluate CV risk stratification in patients with T2D.

Background and Objectives: Diabetic peripheral neuropathy (DPN) is a common and debilitating complication of obesity and type 2 diabetes (T2D) affecting up to 50% of patients with long-standing disease. While chronic hyperglycemia plays a central role in its pathogenesis, intensive glycemic control provides only partial protection, suggesting the involvement of additional metabolic pathways. The primary objective of this systematic review was to evaluate the role of lipid metabolism disturbances and advanced lipidomic alterations in the development and progression of DPN in patients with obesity and T2D. Secondary objectives included identifying specific lipid species associated with DPN and exploring their potential pathophysiological and clinical implications. Methods: This systematic review included 8 studies that met the inclusion criteria and was conducted according to PRISMA guidelines and registered in PROSPERO/2026/CRD420261288920. Study quality was assessed using the Newcastle–Ottawa Scale. Results: Large population-based cohorts reported a consistent association between hypertriglyceridemia and DPN prevalence, with triglyceride levels >204 mg/dL associated with an approximately 40% increased risk. Lipidomic analysis revealed alterations in acylcarnitine, sphingolipids, and phospholipids. However, the evidence remains limited and heterogeneous, and neuropathy-specific outcomes were insufficiently evaluated in interventional studies. Conclusions: Lipid metabolism disturbances, particularly hypertriglyceridemia and specific lipidomic alterations, may contribute to DPN beyond the effects of hyperglycemia. Although not yet clinically actionable, lipidomic alterations may represent promising future biomarkers and therapeutic targets in DPN. However, the current evidence is limited by heterogeneity and predominantly observational designs. Further well-designed longitudinal and interventional studies are needed to clarify causal relationships and clinical relevance.