This study interprets the 2024 consensus of the International League Against Epilepsy（ILAE）on the diagnosis and treatment of anxiety and depression in children and adolescents with epilepsy，and compares it with other international guidelines.By analyzing the differences in screening methods，diagnostic tools，treatment principles，and long-term management strategies，the study proposes a clinical diagnosis and management protocol. The findings indicate that anxiety and depression in children with epilepsy are often overlooked，emphasizing the critical importance of early identification and intervention.The study also discusses the necessity for family involvement and multidisciplinary management，highlighting the key role of combining psychotherapy with pharmacotherapy in improving patient outcomes.

Neurocritical care conditions are common causes of death and disability in children.In nearly all pediatric neurocritical cases，various immune cells and factors form a complex and dynamic immune-inflammatory network. The imbalance of homeostasis in this inflammatory network system ultimately leads to immune injury. A comprehensive understanding of the occurrence and development process of immune-inflammatory responses in pediatric neurocritical care，along with emphasis on dynamic assessment of immune inflammation，is conducive to precision treatment and personalized treatment，improving the prognosis of pediatric neurocritical care and reducing the medical burden.

For children with severe neurocritical conditions，analgesia and sedation are key components of treatment，ensuring patients’ comfort during their stay in the intensive care unit and promoting neurological function recovery and improving prognosis. However，there are still differences in the management strategies of analgesia and sedation in children worldwide.This article summarizes the assessment and monitoring of analgesia and sedation in children with severe neurocritical conditions，as well as non-pharmacological and pharmacological treatment options，in order to standardize the application and safety assessment of analgesic and sedative drugs in children with severe neurological conditions，and ultimately promote the analgesia and sedation measures to develop towards evidence-based and precise drug treatment in children with severe neurocritical conditions.

Targeted Temperature Management（TTM）is a crucial neuroprotective strategy in pediatric neurocritical care，yet several key problems remain unresolved in its clinical application. Due to immature neurological development，high metabolic rates，and weak thermoregulation，children are more susceptible to secondary brain injury mediated by mitochondrial dysfunction，oxidative stress，and neuroinflammatory responses following acute neurological insults. TTM may exert neuroprotective effects by reducing cerebral metabolism，suppressing inflammation，and inhibiting apoptosis. However，the optimal implementation protocol（e.g.，target temperature，duration，rewarming rate）and the riskbenefit ratio in specific populations require further validation through large-scale clinical studies and long-term follow-up.

Patients in the pediatric neurocritical care（NCC）often require invasive mechanical ventilation due to neurological-related respiratory failure.While guidelines exist for weaning and extubation in ICU patients，there are currently no clear recommendations for weaning and extubation strategies or timing for pediatric NCC patients. This article summarizes current research on weaning，extubation timing，and predictive indicators for pediatric NCC patients. Based on recommendations for ICU and NCC patients in the current guidelines，the timing of weaning and extubation in pediatric NCC patients are explored.

With the promotion and popularization of cardiopulmonary resuscitation technology， the success rate of cardiopulmonary resuscitation has increased; however， the prognosis of patients after cardiopulmonary resuscitation has not been significantly improved.Brain damage is the main cause of death and disability.Therefore，reducing brain damage is the key and difficult point of treatment following cardiac arrest.This paper reviewed the measures of neuroprotection after cardiopulmonary resuscitation.

Viral infection-associated encephalopathy refers to a group of acute brain dysfunction syndromes that occur during or following viral infections，on which no unified international consensus currently exists.In recent years，with advances in the understanding of imaging and immunology，subtypes such as acute necrotizing encephalopathy（ANE）have been gradually recognized. These disorders share common mechanisms，including abnormal immune-inflammatory responses and disturbances in the cerebral microenvironment.In clinical practice，early identification is crucial，and supportive treatment typically involves immunomodulation，blood purification，and neuroprotection.Prognosis varies significantly among different subtypes. Based on the characteristics of pediatric cases， this review explores the pathogenesis，clinical features，imaging characteristics and treatment progress to increase efficiency in recognition and intervention.

Autoimmune encephalitis（AE）is a disease in which autoimmune mechanisms lead to diffuse or multiple inflammatory lesions in the brain parenchyma，resulting in neurological dysfunction. AE combined with related tumors are called paraneoplastic AEs，and the paraneoplastic AE that is consistent with limbic encephalitis is called paraneoplastic limbic encephalitis.The clinical manifestations of pediatric AEs are complex and diverse，and they are very different from adult AEs in terms of clinical disease spectrum，incidence of concomitant tumors，clinical manifestations，disease process，treatment efficacy，and final prognosis. This article summarizes the research progress in the diagnosis and treatment of AEs in children in recent years，aiming to arouse the attention of clinicians to AEs and provide reference for clinical diagnosis and treatment.

Febrile infection-related epilepsy syndrome（FIRES） is a subtype of new-onset refractory status epilepticus（NORSE），characterized by refractory status epilepticus and poor prognosis，and may leave behind severe cognitive andbehavioral dysfunction and drug-resistant epilepsy，etc. In recent years，with the deepening of understanding of this disease，the treatment concept has also changed. It is advocated that on the basis of standardized anti-epileptic seizure treatment，early and timely immunotherapy and comprehensive support should be carried out. This article elaborates on the pathogenesis，clinical manifestations，treatment and prognosis of FIRES，with the aim of enhancing understanding and improving prognosis.

Objective　To summarize the clinical manifestations，genetic features and treatments of children with acute encephalopathy caused by ATP1A2 gene variants，in order to improve the understanding of the disease. Methods　The clinical manifestations, treatment and genetic variant spectrum of eight children with acute encephalopathy caused by ATP1A2 gene variants diagnosed in the Department of Neurology of Beijing Children’s Hospital，Capital Medical University from 2015 to 2024 were retrospectively summarized and analyzed, and the child patients were followed up. Results　There were four males and four females.The age at onset was from 5 months to 5 years 9 months.The causes included fever in eight patients，the intake of large amounts of food in two patients and mild head trauma in one patient. The onset symptoms were coma in five patients and lethargy in three patients（one patient with dysphoria）.The time of symptoms reaching peak was from onset to over 4 days.GTCS occurred in eight patients，hemiplegia occurred in four patients，and aphasia occurred in five patients.None of the eight patients had headache.Disturbance of consciousness lasted from 40 hours to 9 days，and hemiplegia and aphasia lasted from 19 days to 6 months and from 8 days to 26 days，respectively. Previous episodes of encephalopathy ranged from 0 to 6 times. Two patients respectively developed seizure without fever in 1 year 6 months old and 5 years 8 months old. Six patients had recurrent fever and convulsions between 5 months and 2 years 5 months old. Alternating hemiplegia occurred in 2 patients aged from 5 to 10 years old and lasted from 30 minutes to 3 days.Four patients had mild mental retardation.Single or bilateral cerebral cortical cytotoxic edema was shown in cerebral MRI in five patients during acute stage，mild cerebral atrophic changes were shown at recovery stage, and one of them had smaller right cerebral hemisphere，delayed myelination，and a malformed and deepened cerebral fissure in left occipital lobe. Generalized slow wave was observed in EEG in five patients during acute stage；periodic slow wave was observed in two patients; left frontal spike wave，spike slow wave and left frontal-origin subclinical seizures were detected in one patient during recovery stage. Six ATP1A2 gene variants were found in the 8 cases，including four inherited variants and four de novo variants.One novel variant c.2540T>A（p.p.I847N），and two hot spot variants c.2563G>A（p.G855R）and c.2143G>A（p.G715R）were found. Conclusion　Acute encephalopathy in children caused by ATP1A2 gene variants is likely to occur under stress of fever，head trauma，and intake of large amounts of food. The initial symptom is often coma, which is often combined with GTCS, hemiplegia, and aphasia. The course of the disease is reversible and can recur. Generally，headache does not occur in the acute stage, and it is easy to be misdiagnosed as viral encephalitis and cerebral infarction.Avoiding triggering factors and giving symptomatic treatment are the main treatment methods.

Objective　This study aims to summarize and analyze the clinical features，genetic mutation characteristics，and gene-phenotype correlations in five pediatric patients with developmental epileptic encephalopathy caused by CACNA1A gene mutations，in order to provide a basis for early diagnosis，treatment strategy selection，and genetic 
counseling of this condition. Methods　Clinical data，genetic results，and family verification reports were collected in five pediatric patients with developmental epileptic encephalopathy caused by CACNA1A gene mutations admitted to the Department of Neurology of Hebei Children’s Hospital from its establishment（1989） to January 2023. Descriptive analysis was conducted on the patients’ clinical characteristics，mutation types，and other relevant factors. Results　Among the 5 pediatric patients with developmental epileptic encephalopathy，3 were male and 2 were female，with onset ages ranging from 2 months to 6 years and 8 months. Two cases were inherited mutations，while 3 were de novo mutations. There were four cases of missense mutations and one case of nonsense mutation. The initial seizure types varied: three were generalized tonic-clonic seizures，one was a focal seizure，and one was an absence seizure. Among them，one case was a generalized tonic-clonic seizure with status epilepticus complicated by acute encephalopathy. Four patients exhibited generalized developmental delay，while one had normal development. Video EEG findings included 1 case of generalized spike-and-wave activity intermixed with slow waves，1 case of frontal spikes，1 case of multifocal spikes，1 case of generalized spike-and-wave activity intermixed with slow waves，and 1 normal case. Cranial MRI showed that there were 3 normal cases，1 case of demyelination with mild widening of the frontal-temporal subarachnoid space，and 1 case of focal demyelination，bilateral widening of the frontal-temporal subarachnoid space，widening of cerebellar sulci，and bilateral hippocampal swelling. During the 1-year follow-up，seizures resolved in 2 patients while 3 patients continued to experience intermittent seizures. Mutations located in the I-S1 and Ⅳ-S6 regions of the Cav2.1 calcium channel carboxyl-terminal domain resulted in severe phenotypes， whereas mutations in the Ⅳ-S6 and Ⅲ-S2 regions led to mild phenotypes. Software prediction indicated that mutations in children with severe phenotypes diagnosed with drug-resistant epilepsy caused structural alterations in the protein; on the contrary，mutations in children with mild phenotypes did not induce structural changes in the protein. Conclusion　The age of onset of developmental epileptic encephalopathy caused by CACNA1A mutations ranges from infancy to school age. Common seizure types are diverse，with most cases presenting as drug-resistant epilepsy. Severe cases may lead to status epilepticus and acute encephalopathy. The drug-resistant nature of seizures may be related to the location of the gene mutation and the resulting structural alterations in the protein.