Purpose: To evaluate the safety and efficacy of long vascular sheaths for transfemoral neuroendovascular procedures in children. Materials and Methods: A retrospective evaluation of transfemoral neuroendovascular procedures in children <18 years, using long sheaths was undertaken analyzing procedure type, fluoroscopic times, technical success, access site and systemic complications. Twenty-seven consecutive procedures were included over a two-year period. Mean age was 8.4 years (standard deviation [SD] 6.3) (range 17.0 months–16.3 years). Results: Patients were 44% female and mean weight was 35.0 kg (SD 22.8) (range 9.8–72.2 kg). A third of the procedures were performed in ≤15 kg children. The most common procedure was for embolization (n=13, 48.1%) and the most common indication was dual microcatheter technique (52%). The most common device used was the 5 Fr Cook Shuttle sheath. Mean fluoroscopy time was 61.9 minutes (SD 43.1). Of these procedures, 93% were technically successful. Femoral vasospasm, when present, was self-limiting. Complications (3/27, 11.1%) included groin hematoma (n=1), neck vessel spasm that resolved with verapamil (n=1), and intracranial thromboembolism (n=1), with no significant difference between the ≤15 kg and >15 kg subcohorts. There were no aorto-femoro-iliac or limb-ischemic complications. Conclusion Long vascular sheaths without short femoral sheaths can be safely used for pediatric neuroendovascular procedures as they effectively increase inner diameter access without increasing the outer sheath diameter. This property increases the range of devices used and intracranial techniques that can be safely performed without arterial compromise, thus increasing the repertoire of the neurointerventionist.

Purpose: To evaluate the safety and efficacy of long vascular sheaths for transfemoral neuroendovascular procedures in children. Materials and Methods: A retrospective evaluation of transfemoral neuroendovascular procedures in children <18 years, using long sheaths was undertaken analyzing procedure type, fluoroscopic times, technical success, access site and systemic complications. Twenty-seven consecutive procedures were included over a two-year period. Mean age was 8.4 years (standard deviation [SD] 6.3) (range 17.0 months–16.3 years). Results: Patients were 44% female and mean weight was 35.0 kg (SD 22.8) (range 9.8–72.2 kg). A third of the procedures were performed in ≤15 kg children. The most common procedure was for embolization (n=13, 48.1%) and the most common indication was dual microcatheter technique (52%). The most common device used was the 5 Fr Cook Shuttle sheath. Mean fluoroscopy time was 61.9 minutes (SD 43.1). Of these procedures, 93% were technically successful. Femoral vasospasm, when present, was self-limiting. Complications (3/27, 11.1%) included groin hematoma (n=1), neck vessel spasm that resolved with verapamil (n=1), and intracranial thromboembolism (n=1), with no significant difference between the ≤15 kg and >15 kg subcohorts. There were no aorto-femoro-iliac or limb-ischemic complications. Conclusion Long vascular sheaths without short femoral sheaths can be safely used for pediatric neuroendovascular procedures as they effectively increase inner diameter access without increasing the outer sheath diameter. This property increases the range of devices used and intracranial techniques that can be safely performed without arterial compromise, thus increasing the repertoire of the neurointerventionist.

Autoimmune encephalitis (AE) is a category of immune-mediated disorders of the central nervous system (CNS) affecting children and adults. It is characterized by the subacute onset of altered mentation, neurocognitive issues, refractory seizures/ drug-resistant epilepsy, movement disorders, and/or autonomic dysfunction. AE is mediated by autoantibodies targeting specific surface components or intracytoplasmic antigens in the CNS, leading to functional or structural alterations. Multiple triggers that induce autoimmunity have been described, which are mainly parainfectious and paraneoplastic. The imaging features of AE often overlap with each other and with other common causes of encephalitis/encephalopathy (infections and toxic-metabolic etiologies). Limbic encephalitis is the most common imaging finding shared by most of these entities. Cortical, basal ganglia, diencephalon, and brainstem involvement may also be present. Cerebellar involvement is rare and is often a part of paraneoplastic degeneration. Owing to an improved understanding of AE, their incidence and detection have increased. Hence, in an appropriate setting, a high degree of suspicion is crucial when reporting clinical MRIs to ensure prompt treatment and better patient outcomes. In this review, we discuss the pathophysiology of AE and common etiologies encountered in clinical practice.

Autoimmune encephalitis (AE) is a category of immune-mediated disorders of the central nervous system (CNS) affecting children and adults. It is characterized by the subacute onset of altered mentation, neurocognitive issues, refractory seizures/ drug-resistant epilepsy, movement disorders, and/or autonomic dysfunction. AE is mediated by autoantibodies targeting specific surface components or intracytoplasmic antigens in the CNS, leading to functional or structural alterations. Multiple triggers that induce autoimmunity have been described, which are mainly parainfectious and paraneoplastic. The imaging features of AE often overlap with each other and with other common causes of encephalitis/encephalopathy (infections and toxic-metabolic etiologies). Limbic encephalitis is the most common imaging finding shared by most of these entities. Cortical, basal ganglia, diencephalon, and brainstem involvement may also be present. Cerebellar involvement is rare and is often a part of paraneoplastic degeneration. Owing to an improved understanding of AE, their incidence and detection have increased. Hence, in an appropriate setting, a high degree of suspicion is crucial when reporting clinical MRIs to ensure prompt treatment and better patient outcomes. In this review, we discuss the pathophysiology of AE and common etiologies encountered in clinical practice.

Autoimmune encephalitis (AE) is a category of immune-mediated disorders of the central nervous system (CNS) affecting children and adults. It is characterized by the subacute onset of altered mentation, neurocognitive issues, refractory seizures/ drug-resistant epilepsy, movement disorders, and/or autonomic dysfunction. AE is mediated by autoantibodies targeting specific surface components or intracytoplasmic antigens in the CNS, leading to functional or structural alterations. Multiple triggers that induce autoimmunity have been described, which are mainly parainfectious and paraneoplastic. The imaging features of AE often overlap with each other and with other common causes of encephalitis/encephalopathy (infections and toxic-metabolic etiologies). Limbic encephalitis is the most common imaging finding shared by most of these entities. Cortical, basal ganglia, diencephalon, and brainstem involvement may also be present. Cerebellar involvement is rare and is often a part of paraneoplastic degeneration. Owing to an improved understanding of AE, their incidence and detection have increased. Hence, in an appropriate setting, a high degree of suspicion is crucial when reporting clinical MRIs to ensure prompt treatment and better patient outcomes. In this review, we discuss the pathophysiology of AE and common etiologies encountered in clinical practice.

Autoimmune encephalitis (AE) is a category of immune-mediated disorders of the central nervous system (CNS) affecting children and adults. It is characterized by the subacute onset of altered mentation, neurocognitive issues, refractory seizures/ drug-resistant epilepsy, movement disorders, and/or autonomic dysfunction. AE is mediated by autoantibodies targeting specific surface components or intracytoplasmic antigens in the CNS, leading to functional or structural alterations. Multiple triggers that induce autoimmunity have been described, which are mainly parainfectious and paraneoplastic. The imaging features of AE often overlap with each other and with other common causes of encephalitis/encephalopathy (infections and toxic-metabolic etiologies). Limbic encephalitis is the most common imaging finding shared by most of these entities. Cortical, basal ganglia, diencephalon, and brainstem involvement may also be present. Cerebellar involvement is rare and is often a part of paraneoplastic degeneration. Owing to an improved understanding of AE, their incidence and detection have increased. Hence, in an appropriate setting, a high degree of suspicion is crucial when reporting clinical MRIs to ensure prompt treatment and better patient outcomes. In this review, we discuss the pathophysiology of AE and common etiologies encountered in clinical practice.