Autoimmune encephalitis (AE) is a group of inflammatory disorders caused by immune-mediated attacks on the central nervous system, with common clinical manifestations including psychiatric and behavioral abnormalities, cognitive and motor impairments and epileptic seizures. Conventional first-line therapies mainly rely on corticosteroids, intravenous immunoglobulin, and plasma exchange. However, a subset of patients exhibits suboptimal responses or high relapse rates, underscoring the urgent need for the development of novel therapeutic strategies. In recent years, targeted therapeutic approaches have advanced rapidly in the field of AE, primarily focusing on key immune components such as B cells, T cells, the complement cascade, and key inflammatory cytokines. Anti-CD20 monoclonal antibodies have demonstrated promising efficacy in refractory AE. Moreover, emerging agents such as ocrelizumab, epratuzumab, telitacicept, and daratumumab have provided refined strategies for the precise depletion of B cells and plasma cells. In parallel, cytokine-targeting biologics, Janus kinase inhibitors, and the proteasome inhibitor bortezomib have shown potential value for modulating aberrant immune responses. In addition, chimeric antigen receptor (CAR)-T cell immunotherapy is gradually emerging as an important frontier in exploratory research. Looking ahead, by integrating neurorestorative strategies with artificial intelligence-assisted diagnostic and therapeutic decision-making, targeted therapies are expected to drive AE management from traditional empirical immunosuppression toward a new era of precision intervention, thereby enabling more efficient and personalized disease management.
Epilepsy is a chronic neurological disorder often complicated by drug resistance and comorbidities, with limited benefits from conventional therapies. This review explores the role of neuro-immune interactions in epilepsy, detailing a core mechanism where seizures disrupt the blood-brain barrier, enabling immune cell infiltration and activating glial cells to release pro-inflammatory factors, thus perpetuating a vicious cycle. Key signaling pathways are also discussed. The article surveys diagnostic advances, including neuro-immune biomarkers and technologies like multimodal imaging and single-cell sequencing. For treatment, immunomodulatory strategies—such as targeting inflammation, modulating glial cells or gut microbiota, and cell therapies—as well as the development of novel anti-seizure medications are summarized. Current challenges involve controversies over immune cell functions and inflammatory causality, as well as limitations in animal models and clinical translation. Future directions like multi-omics integration, artificial intelligence, and novel delivery systems are highlighted, offering a new paradigm for precise, etiology-targeted therapy in drug-resistant epilepsy.
Hereditary epilepsy refers to a type of epilepsy in which seizures are directly triggered by genetic defects and constitute the core clinical manifestation of the disease. In recent years, with the rapid advancement of gene detection technologies, the genetic mechanisms associated with epilepsy have been progressively elucidated, thereby driving progress in the precision diagnosis and treatment of the condition. Genetic testing has become a crucial tool for the clinical diagnosis and management of hereditary epilepsy. Based on in-depth analysis of specific gene mutations and pathogenic mechanisms, more targeted individualized treatment plans can be developed for patients. This article aims to focus on the etiological classification of hereditary epilepsy and the latest research advances in its precision diagnosis and treatment. Overall, the prospects for precision medicine in hereditary epilepsy are promising. Moving forward, continued multidisciplinary collaboration and sustained efforts are needed to further integrate genetics into clinical practice for epilepsy.
Social cognition is a core ability that enables individuals to recognize others' emotions and intentions and relies on a highly coordinated social brain network (SBN), which includes key brain regions such as the fusiform gyrus, amygdala, and medial prefrontal cortex. As a network disorder, epilepsy not only causes seizure manifestations but also disrupts the structure and function of the SBN through direct involvement of epileptogenic foci or the remote propagation of abnormal discharges, leading to social cognitive impairments such as difficulties in emotion recognition, deficits in theory of mind, impaired empathy, and abnormalities in social decision-making. Children and adolescents with epilepsy are particularly vulnerable to deviations in social cognitive development because their brain networks are still undergoing maturation. This review systematically elaborates on the neural underpinnings and clinical manifestations of the SBN in epilepsy, as well as its developmental characteristics in children and adolescents, and proposes a clinically translatable pathway from assessment to intervention. Furthermore, it emphasizes the integration of neuroimaging, neuropsychological assessment, and multimodal rehabilitation strategies to promote a paradigm shift in epilepsy management from seizure control to the improvement of social functioning.
Epilepsy is a common chronic brain disorder, with approximately 30% of patients being resistant to conventional anti-epileptic drugs, necessitating precision medicine strategies for individualized treatment. This article systematically reviews the key advances and future directions in the precision treatment of epilepsy, , with its core framework built on three main pillars. First, targeted therapies based on genetic etiology serves as the cornerstone of precision medicine. By using genetic diagnostics to identify pathogenic mutations (such as in SCN1A and KCNQ2), treatment strategies can be tailored with channel modulators, receptor antagonists, or ketogenic diets that address the underlying causes. Second, pharmacogenomics aids in the personalized selection of conventional anti-epileptic drugs by analyzing key genes such as CYP2C9 and HLA-B*15:02, effectively predicting therapeutic efficacy and preventing severe adverse reactions. Third, for drug-resistant epilepsy, precision surgical techniques and neuromodulation methods accurately localize the epileptogenic focus, providing effective intervention options for patients. In the future, integrating multi-omics data, developing of novel targeted therapies, and overcoming clinical translation bottlenecks will be crucial in making precision treatments accessible to a broader patient population.
Objective: To investigate the neurological clinical manifestations, diagnosis, and key treatment strategies of acute intermittent porphyria (AIP), with the aim of improving early recognition and standardized management of the disease.
Methods: The clinical data of a patient who presented with abdominal pain and seizures at disease onset was reported, and a literature review regarding the clinical features, pathogenesis, diagnosis, differential diagnosis, and treatment of AIP was conducted.
Results: The patient successively developed acute abdominal pain, epileptic seizures, and predominantly proximal motor axonal neuropathy. Urinary porphobilinogen (PBG) levels were significantly elevated, and genetic testing revealed a heterozygous mutation in the hydroxymethylbilane synthase (HMBS) gene.
Conclusion: The neurological manifestations of AIP exhibited a characteristic temporal pattern of evolution, and urinary PBG screening is crucial for early diagnosis. Early initiation of hemin therapy is essential to halt disease progression and improve clinical outcomes.
Epilepsy is a chronic brain disease characterized by central nervous system dysfunction, and its frequent seizures have a serious impact on the quality of life for patients. At present, the primary treatment is based on Western anti-epileptic medications; however, long-term use of these drugs can lead to a series of adverse reactions. Chaihu Jia Longgu Muli Decoction, mentioned in Article 107 of the On Cold Damage (Shang Han Lun), has been commonly used by both ancient and modern physicians to treat mental and emotional diseases such as "chest fullness and agitation". In recent years, many studies have shown that this formula has a significant efficacy in treating epilepsy. Chaihu Jia Longgu Muli Decoction can exert its anti-epileptic effects by regulating neurotransmitters, enhancing the function of central nervous systems cells, and modulating inflammatory markers. This formula serves multiple functions, including harmonizing the Shaoyang, Tongyang Xiezhuo, and tranquilizing mind. Its effects are multi-targeted and systemic in nature. In the clinical treatment of patients with epilepsy, Chaihu Jia Longgu Muli Decoction has played an important role. This article offers a comprehensive overview of the recent developments regarding this formula's application in epilepsy treatment, focusing on the prescription compatibility, its underlying mechanisms of action, and relevant clinical observations.
Objective： To evaluate the effects of botulinum toxin type A (BTX-A) injection combined with serial plaster casting on fine motor function and upper limb spasticity in children with spastic cerebral palsy (CP).
Methods： A total of 119 children with CP were stratified according to clinical subtype and Manual Ability Classification System (MACS) level, and then randomly divided into an experimental group (n=61) and a control group (n=58) using a random number table. The control group received a single BTX-A injection combined with conventional upper limb rehabilitation training and guidance. The experimental group received additional serial plaster casting. Therapeutic effects were assessed using the Fine Motor Function Measure (FMFM) and the Modified Tardieu Scale (MTS), which assessed spasticity using parameter X, before BTX-A injection, at 1 month, and at 3 months after injection.
Results： At 1 month after treatment, FMFM scores and MTS parameter X scores significantly improved in both groups (P < 0.05), with the experimental group showing superior outcomes compared to the control group (P < 0.05). At 3 months, all scores in the experimental group remained improved despite a slight decrease, while in the control group, all indicators except for elbow extension showed no statistically significant difference compared to those at 1 month post-treatment.
Conclusion： BTX-A combined with conventional upper limb rehabilitation training can significantly improve upper limb muscle spasticity and large-joint motor function in children with CP. The addition of serial plaster casting helps to further enhance hand function and prolong the therapeutic effect.
Post-stroke depression (PSD) is one of the most common neuropsychiatric complications following stroke, with a high incidence rate. Depressive states inhibit the secretion of brain-derived neurotrophic factors and hinder neural repair. Early identification and intervention of PSD are crucial for patients' functional recovery, quality of life, and prognosis. Antidepressants can significantly improve depressive symptoms, and early use of antidepressants can also improve patients' motor and cognitive functions. Combining pharmacotherapy with exercise therapy and occupational therapy can enhance the effectiveness of drug treatment. Early intervention for PSD can correct patients' negative cognition towards post-stroke dysfunction, reduce the risk of depressive relapse, and avoid long-term psychosocial impairment.
Objective: To evaluate the effectiveness of integrating the evidence-based medicine (EBM) PICOS framework with case-based learning (CBL) in the teaching of neurorehabilitation.
Methods: A total of 100 third-year undergraduates majoring in rehabilitation therapy at Changsha Medical University (Class of 2021) were randomly assigned into two groups through stratified randomization: a reform group and a control group, with 50 students in each. In the neurorehabilitation course, the control group received traditional teaching methods (lecture-based learning), while the reform group was taught using the EBM-PICOS framework combined with CBL. After course completion, teaching effectiveness was compared between the two groups across three dimensions: academic performance, learning outcomes, and clinical internship adaptability.
Results: Compared with the control group, the reform group demonstrated statistically significant improvements in academic performance and clinical internship adaptation scores (P<0.05). The reform group also showed superior learning outcomes in seven aspects: learning engagement, self-directed learning competency, evidence-based practice proficiency, literature retrieval skills, clinical reasoning ability, applied knowledge integration, and professional identity (all P<0.05). However, no statistically significant difference was observed in medical ethics and professionalism between the two groups (P>0.05).
Conclusion: The integration of the EBM-PICOS framework with CBL enhances teaching effectiveness in neurorehabilitation and effectively cultivates rehabilitation competency among rehabilitation therapy students.
This article reports a case of an elderly female who presented with instability in standing and walking. She had a long-term vegetarian diet and experienced nutritional deficiency in the three months preceding onset. Cervical spinal MRI revealed an "inverted V sign" in the posterior columns. Based on the patient's symptoms, signs, auxiliary examinations, and treatment follow-up results, a final diagnosis of subacute combined degeneration was made. By reviewing the pathophysiological mechanism of the "inverted V sign" as a distinctive imaging manifestation, this article explores the differential diagnostic considerations for this radiological finding.
