This article reports a case of delayed oculomotor nerve palsy after basal ganglia hemorrhage breaking into the ventricles and discusses its clinical features and possible pathogenic mechanisms，so as to provide a reference for clinical diagnosis and treatment. A retrospective analysis was performed for the clinical data of a male patient with intracerebral hemorrhage aged 57 years，including medical history，physical examination，imaging examination，diagnosis，and treatment，and the possible pathogenic mechanisms were analyzed with reference to related articles in China and globally. Head computed tomography angiography showed no signs of aneurysm. The patient achieved absorption of intracerebral hemorrhage after treatment and complete resolution of blepharoptosis and recovery of eye movement at 2 months after discharge. Delayed oculomotor nerve palsy may occur after intracerebral hemorrhage breaking into the ventricles，and its pathogenesis may be associated with factors such as nerve compression caused by organization and contraction of intraventricular blood clots and vasospasm. Conservative treatment may help to achieve a good prognosis. This case can provide a reference for clinical practice.

Migraine is a neurovascular disorder and ranks as the second leading cause of disability worldwide. The Global Burden of Disease Study 2021 estimated that approximately 1.2 billion people are affected by migraine，making it one of the major contributors to years lived with disability years attributable to neurological disorders. The pathogenesis of migraine is complex and involves multiple processes，including activation of the trigeminovascular system，neuroinflammation，abnormal meningeal vasomotion，and central sensitization. Among these，potassium channels play a vital role in maintaining the resting membrane potential of cells，regulating neuronal excitability，modulating neurotransmitter release，and controlling vascular tone. In recent years，the inwardly rectifying potassium channel （Kir） family has become a hotspot in headache research. This family includes Kir2.x，G protein-coupled inwardly rectifying potassium channels （GIRK/Kir3.x），and ATP-sensitive potassium channels （K_ATP，Kir6.x/SUR），which are involved in membrane potential stabilization，receptor-coupled inhibition，spatial potassium buffering in glial cells，and metabolic-electrical activity coupling. Notably，the K_ATP channel opener levcromakalim can reliably induce migraine attacks in humans，making K_ATP channels one of the most translationally promising ion channel targets at present. This article focuses on the role of inwardly rectifying potassium channels in migraine，summarizes the distribution，mechanisms，and physiological functions of various Kir channels，and discusses the evidence supporting the involvement of the Kir family in migraine. Furthermore，it reviews the interactions among different Kir channels，as well as their crosstalk with canonical migraine pathways including CGRP，PACAP，and NO. Finally，it analyzes relevant therapeutic targets，current research limitations，and future directions. Overall，inwardly rectifying potassium channels are situated at critical nodes of functional coupling among neurons，glial cells，and vascular smooth muscle，representing an important entry point for understanding migraine heterogeneity and developing precision therapeutics.

Vestibular migraine （VM） is not only a common cause of episodic vertigo but also a systemic disorder involving extensive brain network dysfunction. In addition to typical headache and severe vestibular symptoms，VM is often accompanied by significant cognitive alterations that seriously impair the daily functioning and social capacity of patients. This article systematically reviews the latest research advances in VM-associated cognitive impairment in terms of clinical phenotypes，potential pathophysiological mechanisms，biomarkers，and assessment scales. Clinical assessments show that VM-associated cognitive impairment mainly manifests as retardation of thinking，impaired attention and working memory，increased cognitive load，and impaired executive function，as well as a potential increase in the risk of falls. Neuroimaging and neuroelectrophysiological evidence has revealed the presence of microstructural damage along with macroscopic functional network reorganization and structural alterations in the brains of VM patients. Besides，5-hydroxytryptamine，calcitonin gene-related peptide，macrophage migration inhibitory factor，and 25-OH vitamin D may participate in the development and progression of VM-associated cognitive impairment. In conclusion，through a comprehensive assessment of scales，neuroimaging，electrophysiological examination，and serological biomarkers，cognitive screening in VM patients can achieve early detection of cognitive dysfunction，and effective interventions should be performed to control the symptoms of VM while protecting cognitive function，so as to improve long-term prognosis and quality of life for these patients.

Migraine is a common disabling trigeminovascular disorder，and its comorbidity with ocular diseases has attracted increasing attention in clinical practice. This review focuses on the comorbid relationship between migraine and dry eye disease，constructs a whole-process clinical management pathway，emphasizes the core value of multidisciplinary team collaboration between ophthalmology and neurology in optimizing patient prognosis，and points out that prospective multicenter studies are needed in the future to further reveal the mechanism of such comorbidity and explore biomarkers and novel targeted therapies，so as to improve the long-term quality of life of patients with this comorbidity.

Cluster headache（CH） is a severe primary headache disorder characterized by excruciating pain，with a complex pathophysiology involving intricate interactions among the trigeminovascular system，the hypothalamic circadian clock，and the autonomic nervous system. In recent years，calcitonin gene-related peptide （CGRP），recognized as a core mediator in migraine pathophysiology，has also attracted substantial attention regarding its role in CH. This review aims to thoroughly dissect the central role of CGRP in the pathogenesis of CH，systematically elaborate on the relationship between the circadian rhythmicity of CH attacks and the regulation of CGRP pathways，and，through differential diagnostic analysis of CH versus other trigeminal autonomic cephalalgias，reveal the distinct roles of CGRP pathways across different headache subtypes. By integrating the latest preclinical studies，clinical trial data，and biomarker explorations，this article seeks to provide a comprehensive reference for understanding the complex pathophysiology of CH and for developing novel targeted therapeutic strategies.

Migraine is a common primary headache disorder with a high disability burden，and temporomandibular disorders （TMD） are among the most prevalent chronic pain conditions in the orofacial region. Studies have shown a significant bidirectional comorbidity between migraine and TMD，with pain-related TMD being particularly closely associated with migraine. Patients with this comorbidity often experience greater pain burden，more pronounced psychological distress，and poorer quality of life. The underlying mechanisms may involve multiple factors，including the convergence of pain signals within the trigeminal system，peripheral and central sensitization，abnormal neuropeptide signaling involving calcitonin gene-related peptide，oral parafunctional behaviors，sleep disturbances，and psychological stress. The third edition of the International Classification of Headache Disorders （ICHD-3） classifies “headache attributed to temporomandibular disorder” as an entry for secondary headache diagnosis. Clinically，attention should be paid to differentiating migraine comorbid with TMD from TMD-related secondary headache. This review focuses on the epidemiological association，potential comorbid mechanisms，diagnostic differentiation，and oral clinical implications of migraine and TMD，aiming to provide a reference for the standardized identification and comprehensive management of affected patients.

Objective To investigate the association of the polymorphisms of vitamin D receptor ApaI and BsmI genes with the risk of vestibular migraine（VM）. Methods A retrospective case-control study was conducted. A total of 200 patients with VM who were admitted to The Affiliated Xuzhou Municipal Hospital of Xuzhou Medical University from April 2024 to June 2025 were enrolled as VM group，and 100 healthy individuals who underwent physical examination in the same hospital during the same period of time were enrolled as control group. Peripheral blood DNA samples were collected from all subjects to investigate the polymorphisms of the ApaI gene at the rs7975232 locus and the BsmI gene at the rs1544410 locus，and the genotype and allele frequencies at these loci were analyzed for both groups，as well as their association with the onset of VM. Results There were significant differences between the VM group and the control group in the genotype distribution of the ApaI gene at the rs7975232 locus and the BsmI gene at the rs1544410 locus（P<0.05），and compared with the control group，the VM group had a significantly higher frequency of A allele at the rs7975232 locus of the ApaI gene and a significantly higher frequency of G allele at the rs1544410 locus of the BsmI gene（P<0.05）. Compared with the control group，the VM group had a significantly higher proportion of patients with a family history of migraine and significant increases in the levels of total cholesterol and serum uric acid（P<0.05）. The Logistic regression analysis showed that a family history of migraine，a high level of serum uric acid，the AA genotype at the rs7975232 locus of the ApaI gene，and the GG genotype at the rs1544410 locus of the BsmI gene were risk factors for the onset of VM（odds ratio>1，P<0.05）. Conclusion The AA genotype at the rs7975232 locus of the ApaI gene and the GG genotype at the rs1544410 locus of the BsmI gene may be associated with the susceptibility to VM. Detection of the genotypes of these two genes can help to assess the risk of VM.

Trigeminal autonomic cephalalgias（TACs）are a group of primary headache syndromes characterized by unilateral headache and ipsilateral craniofacial autonomic symptoms. TACs include cluster headache，paroxysmal hemicrania，short-lasting unilateral neuralgiform headache attacks（including short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing and short-lasting unilateral neuralgiform headache attacks with craniofacial autonomic symptoms），and hemicrania continua. The pathophysiology involves the trigeminovascular system，the autonomic nervous system，the hypothalamus，and the recently identified role of the vagus nerve. Diagnosis mainly relies on headache attack frequency，duration，and accompanying symptoms. Each TAC has its unique clinical manifestations，pathophysiology，and treatment methods，which are discussed in depth in this review.

Migraine，as a globally high-burden neurological disorder，imposes a dual burden on individual quality of life and the public health system due to its high prevalence rate，high misdiagnosis rate，and significant disability during attacks. Traditional diagnosis and treatment modes face problems such as a lack of individualized treatment regimens，the difficulty in predicting attacks，insufficient objective basis for diagnosis，and the risk of excessive drug use. In recent years，machine learning-based research methods have shown strong potential in integrating clinical data，thereby providing new research ideas for the precise prediction，diagnosis and classification，and individualized treatment decision-making of migraine. This article reviews the application of machine learning in migraine in recent years.

Primary headaches，particularly migraine and tension-type headache，are among the leading causes of disability worldwide. This article systematically reviews recent international and domestic advances in the field of nursing care for primary headaches and elaborates on the critical role of nurses in the comprehensive management of headaches. Evidence indicates that nurses serve as a vital bridge connecting patients with the healthcare system，coordinating multidisciplinary teams，and facilitating patient self-management. In terms of nursing assessment，headache nurses perform systematic history taking，physical and psychological evaluation，and psychosocial assessment to lay the foundation for individualized care plans. Regarding treatment implementation，headache nurses are responsible for monitoring adverse reactions to acute-phase and preventive medications as well as for preventing and monitoring medication-overuse headache. In terms of non-pharmacological interventions，headache nurses lead the delivery of multifaceted measures including lifestyle modification，cognitive behavioral therapy，biofeedback，and health education. Of particular importance，headache nurse-led health education models，through headache diary management，digital tool applications，and multidisciplinary collaboration，significantly enhance the disease awareness，treatment adherence，and self-efficacy of patients. In the future，establishing headache nurse-led headache centers and community-based nursing systems will shift headache management from passive symptom control toward active functional rehabilitation and improvement of quality of life.

Epilepsy is a neurological disorder with marked genetic heterogeneity， and genetic factors play an important role in the development and progression of epilepsy. High-throughput sequencing， genome-wide association studies， and large-scale genomic databases have greatly accelerated the discovery of epilepsy-associated genes and precision medicine； however， the pathogenic interpretation of low-frequency variants， complex inheritance patterns， and variants with mild functional impairment remains challenging. The gene dependency principle addresses how life activities depend on gene function and proposes the key concepts including functional dependency， genetic dependent nature， genetic dependent quantity， and genetic dependent stage， which provides a new medical genetics framework for understanding gene-disease relationship and the pathogenicity of variants.Based on this principle， the 3-Ⅰ approach emphasizes individualized phenotype analysis， individualized case analysis， and individualized gene analysis， integrating whole-exome sequencing， gene dependency assessment， and the China Epilepsy Gene 1.0 Project cohort， and this framework has facilitated the discovery or identification of more than 40 novel pathogenic genes or candidate pathogenic genes for epilepsy， thereby providing a theoretical basis for precise diagnosis， individualized therapy， genetic counseling，and disease prevention.Recently， the new pathogenic gene phenotypes including USP25， ZFHX3， and ATP6V0C have been recognized by OMIM， which fully reflects the application value of the gene dependency principle in the discovery of novel epilepsy-associated genes.

This article summarizes the research advances in the clinical manifestations， related factors， and underlying mechanisms of cognitive impairment in elderly adults with epilepsy. The prevalence rate of cognitive impairment ranges from 26% to 87% in elderly adults with epilepsy， with the main manifestations of impairment in short- and long-term visual memory， verbal memory， executive function， attention， and psychomotor speed. Cognitive function in elderly adults with epilepsy shows a progressive decline over time， which can be explained by the parallel decline model， the two-hit model， and the accelerated aging model. Epilepsy comorbid with cognitive impairment in elderly adults may result from the combined effect of epilepsy itself， brain structural and functional changes， comorbidity burden， anti-seizure medications， and pathological changes associated with Alzheimer disease. Frequent seizures and subclinical epileptiform discharges may accelerate cognitive decline by disrupting neural network activity and memory consolidation processes. The bidirectional relationship between epilepsy and dementia suggests the existence of shared pathological mechanisms leading to cognitive impairment.

Electroencephalography（EEG） is a fundamental tool in the diagnosis and management of epilepsy， and in recent years， its role in epilepsy associated with malformations of cortical development（MCD） has expanded from a conventional tool for adjunctive diagnosis to one used to reveal structural etiologies and assess prognosis. This article systematically reviews the scalp EEG features of patients with MCD， summarizes the electrophysiological manifestations of common MCD subtypes， and highlights the value of EEG in the diagnosis of MCD and the potential significance of its discharge patterns in prognostic evaluation， in order to provide a reference for clinical diagnosis and treatment.

Epilepsy is a common chronic nervous system disease worldwide， affecting approximately 50 million people around the world. Some patients have shown poor response to existing anti-seizure medications and neuromodulation therapies， and therefore， it is urgently needed to explore new treatment strategies. Polyunsaturated fatty acid（PUFA） have become a research hotspot in the field of nutritional intervention for epilepsy due to their roles in neural signaling， cell membrane stability， and inflammation regulation. Studies have shown that ω-3 fatty acids can reduce neuronal excitability， inhibit inflammatory response， and improve mitochondrial energy metabolism， whereas metabolic imbalance of ω-6 fatty acids may activate inflammatory pathways and exacerbate neuronal injury. PUFA may regulate the PPARγ/AMPK/NF-κB signaling axis， thereby coordinating inflammation and energy metabolism through immunometabolic coupling， maintaining neuroimmune homeostasis， and optimizing cerebral energy supply.On this basis， optimizing the composition of PUFA and ω-6/ω-3 ratio in ketogenic diet may become an effective supplementary strategy for epilepsy management， particularly offering a new nutritional intervention approach for medically intractable epilepsy， with important clinical and translational value.

Objective To analyze the changing trends of the incidence and mortality of epilepsy in China from 1994 to 2023， and to provide a basis for the formulation of prevention and control strategies. Methods Based on the research database of the Global Burden of Disease Study 2023（GBD 2023）， the data on the incidence and mortality of epilepsy in China from 1994 to 2023 were extracted， and the age-period-cohort model was used to estimate the age， period， and cohort effects on the risk of onset and mortality of epilepsy. Meanwhile， the ARIMA model was used to predict the changing trends of the incidence and mortality rates of epilepsy from 2024 to 2030. Results The results of age effect analysis showed that the incidence rate of epilepsy in China from 1994 to 2023 first decreased and then increased with the increase in age， while the mortality rate of epilepsy tended to decrease from 5-9 years of age to 65-69 years of age and slightly increase from 70-74 years of age to 85-89 years of age. The highest incidence and mortality rates of epilepsy were observed in the population aged 5-9 years in China， with a peak incidence rate of 34.10/100 000 and a peak mortality rate of 3.9/100 000. The results of period effect analysis showed that the risk of onset first increased， then decreased， and increased again from 1994-1998 to 2009-2013， followed by a reduction from 2009-2013 to 2019-2023； the risk of death tended to decrease from 1994 to 2023， decreasing from 1.30（95%CI 1.26‒1.34） in the period of 1994-1998 to 0.62（95%CI 0.60‒0.64） in the period of 2019-2023. The results of cohort effect analysis showed that the mortality risk of epilepsy in China tended to decrease across successive birth cohorts， with more recent birth cohorts experiencing lower mortality risk. The prediction results showed that the incidence and mortality rates of epilepsy would decrease slowly from 2024 to 2030. Conclusion The incidence and mortality of epilepsy in China are influenced by age effects， period effects， and cohort effects to varying degrees. It is important to focus on the younger and older age groups and implement targeted public health interventions， so as to further reduce disease burden.

Sengers syndrome is a rare autosomal recessive mitochondrial DNA depletion syndrome and a highly malignant disease. Acylglycerol kinase（AGK） is an mitochondrial inner membrane protein that performs both kinase-independent and kinase-dependent functions within the mitochondria， and loss-of-function mutations in AGK are pathogenic factors for Sengers syndrome. This article reports the first case of adult-onset Sengers syndrome comorbid with epilepsy caused by an AGK gene mutation in China and explores the potential mechanisms of seizures， so as to further deepen the understanding and research of the AGK gene and provide a reference for clinical diagnosis and treatment.

Temporal lobe epilepsy（TLE） is one of the most prevalent types of focal epilepsy in clinical practice， and 30%‒40% of these patients progress to refractory temporal lobe epilepsy（RTLE）， while electroencephalography（EEG） is an important cornerstone for the diagnosis and preoperative evaluation of epilepsy. With the continuous advances in neurophysiology and signal analysis technologies in recent years， the understanding of EEG characteristics in RTLE has gradually evolved from traditional spike identification to new dimensions such as high-frequency oscillation analysis and network dynamics interpretation. This article systematically reviews the features of RTLE on scalp and intracranial EEG， clarifies their clinical value in localization of epileptic foci， pathological correlation， and prognostic assessment， and discusses the future developmental trends of related technologies.

Burst suppression is a serious abnormal phenomenon on electroencephalogram（EEG），which often indicates a poor prognosis for patients. This article reports the evolution of EEG burst suppression in a patient with advanced malignant tumor complicated by epilepsy secondary to Listeria meningoencephalitis in the intensive care unit， as well as the diagnosis and treatment process of this patient. This case shows that EEG plays an important role in monitoring the condition of critically ill patients and can provide guidance for diagnosis and treatment.

Objective To investigate the characteristics of choroid plexus volume （CPV） in Alzheimer disease （AD） and mild cognitive impairment （MCI）， as well as its association with cognitive function and the pathological burden of β-amyloid （Aβ） and tau. Methods The data of this study consisted of two parts. The first part of the data were collected from the individuals who attended the memory clinic of The First Hospital of Jilin University from January 2018 to July 2024， among whom there were 142 patients with AD， 95 with MCI， and 85 healthy controls. All individuals underwent neuropsychological assessments and three-dimensional T₁-weighted magnetic resonance imaging. FreeSurfer 7.4.1 combined with a Gaussian mixture model was used to measure CPV， which was then normalized by intracranial volume （ICV）， and the regression analysis and the generalized linear mixed model were used to investigate the association between CPV and cognitive function， as well as longitudinal cognitive changes. The second part of the data were longitudinal data obtained from the Alzheimer Disease Neuroimaging Initiative （ADNI） database； CPV and standardized uptake value ratios （SUVR） of Aβ and tau on PET-CT were extracted， and the generalized linear mixed model was used to observe the effect of CPV on the dynamic changes of Aβ and tau deposition. Results The AD and MCI groups had a significantly higher CPV/ICV ratio than the healthy control group， and the AD group had a significantly higher ratio than the MCI group （P<0.001）.After adjustment for confounding factors， CPV was negatively correlated with Mini-Mental State Examination score and Montreal Cognitive Assessment （MoCA） score and was positively correlated with Clinical Dementia Rating-Sum of Boxes score（P<0.001）. Right-side CPV predicted a longitudinal reduction in MoCA score （β=-2.596， P=0.041） and showed a significant interaction with time （β=-0.166，P=0.013）. In the ADNI cohort， CPV was correlated with Aβ across multiple brain regions and Braak stage and was positively correlated with the SUVR of tau （P<0.05）. Conclusion CPV increases with progression of AD continuum and is associated with cognitive impairment and the deposition of Aβ and tau，suggesting that CPV may be used as a potential low-cost imaging biomarker for AD.

Alzheimer disease （AD） is mainly characterized by progressive cognitive decline， with the core pathological changes of abnormal deposition of amyloid-β（Aβ） and tau protein in the brain. There are currently limited treatment methods for AD， with an urgent need for early risk biomarkers that can be targeted. Triglyceride-glucose （TyG） index is calculated based on fasting blood glucose and triglyceride， and it is an easily accessible surrogate marker for insulin resistance and can reflect metabolic stress load associated with glucose-lipid toxicity. Existing studies have shown that an increase in TyG is associated with cognitive decline and an increase in the risk of dementia or AD， and it may also be associated with core AD biomarkers such as Aβ42 and tau and p-tau in cerebrospinal fluid and atrophy in susceptible brain regions such as the hippocampus.Potential mechanisms may involve the pathways such as impaired brain energy metabolism， blood-brain barrier/neurovascular unit dysfunction， and amplification of neuroinflammation. This article reviews the advances in the clinical and mechanistic research on the association of TyG index with the clinical manifestations and pathological changes of AD and explores its application prospect in longitudinal risk stratification and early prevention of AD.