Venous thromboembolism (VTE) was once considered rare in the young, but it has become an increasingly important complication of contemporary pediatric care, driven by the improved survival of children with complex chronic illness and by the expanding use of central venous catheters. This narrative review synthesizes current evidence on VTE across the entire pediatric age range, from the critically ill neonate to the injured adolescent. We first examine noncerebral VTE in children beyond the newborn period, describing an incidence that is far lower than in adults yet rising among hospitalized patients, the multifactorial risk factors dominated by central venous catheters, and the age-dependent protection conferred by developmental hemostasis. We outline a diagnostic approach centered on compression ultrasonography and computed tomography pulmonary angiography, and a treatment paradigm that increasingly favors direct oral anticoagulants and shorter, six-week courses for low-risk provoked events. Dedicated sections address the distinct biology, presentation, and management of neonatal thrombosis, including renal vein thrombosis, portal vein thrombosis, and purpura fulminans, for which low-molecular-weight heparin is preferred and warfarin is generally avoided. We review the heightened, malignancy-specific risk of cancer-associated thrombosis, the difficulty of anticoagulating the thrombocytopenic child, and the consistent evidence against routine primary thromboprophylaxis. Cerebral sinovenous thrombosis is considered in depth, emphasizing its age-dependent triggers, the central role of magnetic resonance venography, and the safety of anticoagulation. Finally, we summarize the comparatively low but age-graded risk of VTE after major pediatric trauma and the puberty-based approach to prophylaxis. Throughout, we highlight the continued reliance on extrapolated adult data, the emergence of pediatric randomized trials and multicenter registries, and the unmet need for prospectively validated risk-prediction tools. The review offers clinicians an integrated, contemporary framework for recognizing, diagnosing, treating, and preventing thrombosis from the neonate to the adolescent.

Simulation of a human neurological disease on an animal model has the advantage of allowing control and manipulation of most of the regulating factors and producing real biological replicas while, beyond several common traits, every human is dynamic and unique. Moreover, one can explore novel therapeutic strategies on animals before asking permission to apply them to humans. Nevertheless, experimental outcomes depend on species, strain, sex, age, hormonal status, diet, exposure to hypoxia, toxins, radiation, external stimuli, stress, and housing conditions. Further complications stem from tissue hetero-cellularity, technological constraints, computational complexity and difficulties integrating the experimental results into a coherent biological picture. Moreover, most diseases are multi-factorial and associated with altered structure and/or expression of several genes. A major problem with genetically engineered animals is that together with the targeted gene(s), numerous other genes are mutated and/or regulated, owing to their interlinkage in functional pathways. This experience-based methodological commentary presents the challenges, relevance and limitations of the mouse, rat and rabbit models we used to decipher the transcriptomic alterations associated with several neurological disorders. Links to publicly accessible databases presenting experimental protocols and expression profiles are provided for readers interested in reanalyzing our data and comparing them with others' results.

Understanding factors related to early math development is critically important because early math skills predict a number of academic outcomes, such as later math, reading, and school success. Links between spatial and math skills and between executive function and math skills have been established consistently throughout extant research across a variety of ages and skill types. However, little work has examined how these three skillsets are connected; specifically, whether executive function mediates the spatial-math relation. Although past research has found no mediation, this research only included three measures of executive function skills and treated executive function as a single construct, rather than examining the potentially different roles of various executive function skills in the relationship between spatial and math skills. The present study addressed this gap by examining whether five executive function skills (i.e., working memory, inhibitory control, cognitive flexibility, behavioral self-regulation, planning) mediate the relationship between spatial and math skills in preschoolers. Results showed that cognitive flexibility and behavioral self-regulation uniquely mediated this relation, providing preliminary evidence that three specific executive functions (cognitive flexibility, behavioral self-regulation, and planning) mediate the relationship between spatial and math skills. Implications and future directions are discussed.

Congenital thrombotic thrombocytopenic purpura (cTTP) is caused by pathogenic variants in ADAMTS13. Despite the continual expansion of genetic data, there remains no comprehensive, accessible database of ADAMTS13 variation available for clinicians and researchers. We performed a comprehensive literature review and identified 385 ADAMTS13 variants reported in patients worldwide, which were incorporated into an accessible online database to help address this unmet need. Within our database, there is information included on the genetic changes, variant type and effect, clinical features and population allele frequency, to give a thorough and detailed assessment of the variation seen in ADAMTS13. Multiple in silico annotation tools were used to assess coding variation, while AlphaGenome was applied to predict effects of non-coding variation. Variants were distributed throughout the gene, with significant enrichment of variants within the metalloprotease domain. N-terminal variants were associated with earlier age of symptom onset and lower residual ADAMTS13 activity, extending previous genotype-phenotype observations to a larger and more diverse collection of variants. Overall, these findings demonstrate the molecular heterogeneity in cTTP and provide a curated and expandable resource to support variant interpretation, future research, and clinical practice.

The function of the pulvinar, a thalamic structure richly interconnected with the neocortex, is poorly understood. The broad projections from pulvinar to cortex might broadcast common signals across cortical areas. Alternatively, the circuit connecting the cortex and pulvinar might be used to relay activity between cortical areas, complementing the interareal signaling through direct corticocortical circuits. We tested these proposed signaling motifs by performing simultaneous measurements of neuronal population spiking responses in two cortical areas-V1 and V2-and the pulvinar of anesthetized macaque monkeys. We show that corticopulvinar and corticocortical interactions involve distinct patterns of population spiking activity, consistent with the relay hypothesis. Signaling among these structures was biased in the feedforward direction, with V1 activity leading activity in the pulvinar which in turn led V2. Our work suggests that a primary function of the pulvinar is to communicate signals from lower cortical areas to higher areas.

Systemic vasculitis is traditionally classified according to the predominant size of affected vessels; however, phenotypes affecting multiple vascular calibers may not be adequately captured by rigid definitions and require integrated clinicopathological interpretation. Here we report the case of a 70-year-old Caucasian man who presented with persistent systemic inflammation initially suggestive of infection. Although inflammatory markers decreased during antibiotic therapy, residual inflammation persisted, and the subsequent clinical course was characterized by myalgia, pulmonary involvement, and lymphadenopathy. Muscle biopsy revealed noninflammatory myopathic changes, consistent with normal creatine kinase levels. Following the initiation of corticosteroid therapy, the patient rapidly developed purpura and acute nephritic syndrome. Kidney biopsy demonstrated IgA glomerulonephritis (Oxford scores: M0, E0, S0, T0, and C1), interpreted as a manifestation of IgA vasculitis (IgAV), along with sclerosing phase of necrotizing arteritis involving arcuate arteries. These findings demonstrated the coexistence of IgA-mediated glomerular/small-vessel manifestations and chronic medium-vessel arterial pathology but did not establish the exact pathological process leading to the clinical manifestation. Treatment with corticosteroids and cyclophosphamide resulted in rapid clinical remission. This case illustrates a diagnostically challenging vasculitis phenotype involving different vascular compartments that cannot be assigned to a single conventional category. The case highlights the importance of integrated clinicopathological correlation and detailed histopathological assessment in resolving diagnostic uncertainty and guiding immunosuppressive therapy. Recognition of vasculitis as a dynamic disease spectrum rather than a rigidly compartmentalized entity is essential for timely diagnosis and optimal management.

Thrombotic thrombocytopenic purpura (TTP), the most common type of which is immune-mediated (iTTP), is a rare, life-threatening hematologic disorder characterized by thrombocytopenia, microangiopathic hemolytic anemia, and end-organ damage. Prompt recognition and early treatment are essential for survival. Early diagnosis and initiation of treatment are critical in iTTP. Nurses play a key role in recognizing symptoms, supporting patients through treatment, and monitoring for relapse. This review outlines the pathophysiology and clinical presentation of iTTP, along with criteria for diagnosis, with an emphasis on the role of the von Willebrand factor-cleaving protease ADAMTS-13. Current evidence-based treatment strategies are discussed, including therapeutic plasma exchange and immunosuppression with corticosteroids and monoclonal antibody-based therapies. A case study of a middle-aged patient who experienced a relapse of iTTP is presented, illustrating key clinical decision points, challenges in long-term management, and the need for interdisciplinary collaboration.

Splenectomy is a well-established surgical option for selected patients with immune thrombocytopenic purpura and persistent thrombocytopenia despite medical therapy. Although laparoscopic splenectomy remains the standard minimally invasive approach, robotic platforms may offer advantages in technically challenging cases. We present a 40-year-old woman with a 4-year history of immune thrombocytopenic purpura, obesity, Hashimoto thyroiditis, and prior sleeve gastrectomy presented with severe thrombocytopenia and abnormal uterine bleeding. After failure of medical therapy, she underwent robotic splenectomy with the da Vinci Xi robotic platform using an anterior approach. Operative time was 240 minutes, and estimated blood loss was 200 mL. The postoperative course was uneventful, and the patient was discharged on postoperative day 3. Pathologic examination findings were compatible with immune thrombocytopenic purpura. Robotic splenectomy is safe and feasible in this selected challenging case and may be considered an alternative minimally invasive approach when enhanced visualization and precise hilar dissection are desirable.

Graves disease is the most common cause of hyperthyroidism in children. Although neutropenia and thrombocytopenia have been reported in adults with untreated Graves disease, these complications are rare in children. Here, we report a pediatric case of Graves disease complicated by agranulocytosis and thrombocytopenia at diagnosis. A 12-year-old girl presented with increased appetite, irritability, fever, and petechiae. Laboratory examination revealed thyrotoxicosis, and this was associated with agranulocytosis and thrombocytopenia. There was no history of antithyroid drug use. The diagnosis of Graves disease was established based on positive thyroid-stimulating hormone receptor antibodies and thyroid scintigraphy findings. After initiation of a β-blocker and potassium iodide, neutrophil and platelet counts gradually improved in association with the resolution of thyrotoxicosis, which allowed the subsequent introduction of methimazole. The β-blocker and potassium iodide were sequentially discontinued. Blood cell counts remained within the normal range thereafter, and thyroid function has remained well controlled with methimazole monotherapy. This case suggests that thyrotoxicosis itself is associated with cytopenia and provides valuable insight for clinicians when selecting a therapeutic strategy for Graves disease complicated by cytopenia.