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 （KATP，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 KATP channel opener levcromakalim can reliably induce migraine attacks in humans，making KATP 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.
Objective To investigate the association of the serum levels of CXC chemokine ligand 16 （CXCL16） and tumor necrosis factor-α（TNF-α） and the total burden of cerebral small vessel disease （CSVD） with neurological deficit and prognosis in patients with ischemic stroke （AIS）. Methods A total of 120 AIS patients who were hospitalized in Department of Neurology，Shijiazhuang People's Hospital，from December 2022 to January 2024 were enrolled as subjects，and all patients underwent intravenous rt-PA thrombolytic therapy. According to the total burden score of CSVD，the patients were divided into mild-to-moderate burden group with 44 patients and severe burden group with 76 patients. The patients were followed up on day 90 after treatment，and modified Rankin Scale （mRS） used to assess prognosis. According to the prognosis，the patients were divided into good prognosis group with 79 patients and poor prognosis group with 41 patients，and clinical data were compared between the two groups. A Spearman analysis was used to investigate the correlation of the serum levels of CXCL16 and TNF-α with National Institutes of Health Stroke Scale （NIHSS） score and the total burden score of CSVD in all AIS patients；a multivariate Logistic regression analysis was used to investigate the influencing factors for the prognosis of AIS；the receiver operating characteristic （ROC） curve was used to investigate the performance of the serum levels of CXCL16 and TNF-α and the total burden score of CSVD in predicting the prognosis of AIS patients. Results Compared with the mild-to-moderate burden group，the severe burden group had significantly higher serum levels of CXCL16 （P<0.05） and TNF-α （P<0.05），and compared with the good prognosis group，the poor prognosis group had significantly higher serum levels of CXCL16 （P<0.05） and TNF-α （P<0.05）. The serum levels of CXCL16 and TNF-α were positively correlated with NIHSS score （r=0.531 and 0.741，P<0.05） and the total burden score of CSVD （r=0.554 and 0.609，P<0.05）. The poor prognosis group had significantly higher proportions of patients with NIHSS score ≥6 and severe CSVD total burden than the good prognosis group （P<0.05）. NIHSS score ≥6 （OR=2.669，P<0.05），severe CSVD total burden （OR=1.960，P<0.05），CXCL16 （OR=2.219，P<0.05），and TNF-α （OR=2.716，P<0.05） were risk factors for poor prognosis in AIS patients. Serum CXCL16，serum TNF-α，and CSVD total burden score alone had an area under the ROC curve （AUC） of 0.797，0.772，and 0.838，respectively，in predicting the prognosis of AIS patients，while the combination of these three indicators had an AUC of 0.940，with a better performance than each indicator used alone （Zcombination-CXCL16=2.891，Zcombination-TNF-α=4.105，Zcombination-CSVD total burden score=2.847，P=0.003 8，0.001 0，and 0.004 4）. Conclusion The serum levels of CXCL16 and TNF-α and the total burden score of CSVD are associated with neurological deficit and prognosis in AIS patients，and combined measurement of these three indicators has high efficacy in predicting the prognosis of AIS patient.
Objective To investigate the efficacy and safety of endovascular mechanical thrombectomy （EVT） for recanalisation in patients with acute ischaemic stroke （AIS） caused by large vessel occlusion lasting over 24 hours. Methods A retrospective cohort study was conducted on patients with acute ischaemic stroke （AIS） treated with endovascular thrombectomy （EVT） at Jilin Central Hospital between October 2022 and January 2025. Patients were categorised into a time-window group （within 24 hours） and an out-of-time-window group （beyond 24 hours）. Relevant research data （including general information，intraoperative details，and postoperative records） were collected. The primary outcome measure was defined as favourable functional outcome at discharge，specifically a modified Rankin scale （mRS） score of 0-2. Differences between groups were assessed regarding baseline characteristics，intraoperative parameters，and surgical outcomes. Results A total of 293 patients were included，comprising 239 AIS patients within the time window and 54 AIS patients beyond the time window. There was no significant difference in the proportion of favourable outcomes or mortality between patients undergoing EVT within versus beyond the time window （P>0.05）. Conclusion EVT treatment may be safe and effective for AIS patients presenting more than 24 hours after symptom onset.
Objective To investigate the influencing factors for the prognosis of patients with acute basilar artery occlusion after endovascular treatment，as well as the value of collateral circulation scores in predicting prognosis after endovascular treatment. Methods A retrospective analysis was performed for the clinical data of 74 patients with acute basilar artery occlusion who underwent endovascular treatment at Stroke Center of The Affiliated People's Hospital of Henan University of Medicine from January 2020 to June 2025. Modified Rankin Scale （mRS） score on day 90 after surgery was used to assess the prognosis of patients，and then the patients were divided into good prognosis group （47 patients with an mRS score of ≤2） and poor prognosis group （27 patients with an mRS score of >2）. The two groups were compared in terms of baseline data，risk factors，surgical data，infarction location，postoperative complications，pc-ASPECTS score，NIHSS score，and collateral circulation scores （pc-CS and BATMAN）. Results There were significant differences between the two groups in time of operation，NIHSS score，pc-ASPECTS score，pc-CS score，and BATMAN score （P<0.05）. The receiver operating characteristic curve analysis showed that BATMAN and pc-CS had a good performance in predicting the prognosis of patients. Conclusion As the representative methods for assessing collateral circulation，BATMAN and pc-CS have a certain value in predicting prognosis after endovascular treatment for acute basilar artery occlusion，each with its own advantages，and they can be selected based on specific clinical needs.
Objective To investigate the possible mechanism of action of EIF4A3 in nerve injury in rats with cerebral infarction by regulating autophagy through the GSK3β/TFEB pathway. Methods A total of 30 rats were divided into sham-operation group，cerebral infarction group，and EIF4A3 overexpression group，with 10 rats in each group. The double-blind method was used to assess the neurological function of rats；immunofluorescence assay was used to measure the expression of NeuN；TTC staining was used to measure cerebral infarct volume，HE staining was used to observe cerebral histopathological changes，and Nissl staining was used to measure Nissl bodies；Western blotting was used to measure the relative protein expression levels of EIF4A3，GSK3β，TFEB，mTOR，LC3-Ⅱ，and Beclin-1 in brain tissue. Results Compared with the sham-operation group，the cerebral infarction group had an increase in neurological deficit score，a reduction in NeuN expression，and an increase in cerebral infarction volume（P<0.05），as well as disordered structure and cell degeneration/necrosis in brain tissue，reductions in the number of Nissl bodies and the expression levels of EIF4A3 and TFEB in brain tissue，an increase in GSK3β expression （P<0.05），a reduction in the expression level of the autophagy-related protein mTOR，and increases in the expression levels of the autophagy-related proteins LC3-Ⅱ and Beclin-1 （P<0.05）. Compared with the cerebral infarction group，the EIF4A3 overexpression group had a reduction in neurological deficit score，an increase in NeuN expression，a reduction in cerebral infarction volume （P<0.05），alleviation of structural damage of brain tissue，a reduction in the number of degenerated and necrotic cells，and an increase in the number of Nissl bodies，as well as increases in the expression levels of EIF4A3 and TFEB in brain tissue，a reduction in the expression of GSK3β （P<0.05），an increase in the expression level of the autophagy-related protein mTOR，and reductions in the expression levels of the autophagy-related proteins LC3-Ⅱ and Beclin-1 （P<0.05）. Conclusion EIF4A3 can improve nerve injury in rats with cerebral infarction by regulating the GSK3β/TFEB pathway and activating autophagy.
X-linked adrenoleukodystrophy （X-ALD） is an X-linked recessive peroxisomal disorder mainly caused by deficiencies in lysosomal peroxidase，which impairs fatty acid oxidation of very long-chain fatty acids （VLCFA） and leads to the abnormal accumulation of VLCFA in cells and body fluids，finally resulting in the clinical manifestations of diffuse demyelination and adrenal cortical insufficiency.This article reports a case of X-ALD with gait instability as the initial presentation，in order to increase awareness of this rare disease among clinical workers.
To investigate the potential therapeutic value of ofatumumab （OFA） in patients with neuromyelitis optica spectrum disorder （NMOSD） comorbid with Sjögren syndrome （SS）.A retrospective analysis was performed for the clinical data of a patient who was admitted to our hospital on September 21，2022 and was diagnosed with NMOSD and SS，including clinical manifestations，imaging findings，and laboratory results. Under the premise of fully informed consent，the patient received OFA for B-cell depletion therapy to prevent disease recurrence. Disease conditions and adverse events were closely monitored throughout the treatment period.After more than three years of continuous treatment，although the patient developed a pulmonary space-occupying lesion，it did not progress to a malignant disease，and rabies vaccination following a dog bite did not trigger the disease activity of NMOSD or SS. No severe infection was observed during treatment，with satisfactory disease control and a significant improvement in quality of life.This case suggests that OFA may have favorable clinical efficacy and tolerability in patients comorbid with NMOSD and SS，thereby providing a new option for the treatment of such comorbidity. It should be noted that this regimen represents an off-label use，and prospective studies with a large sample size are needed to further validate its efficacy and safety.
Chronic symptomatic middle cerebral artery occlusion is an important factor leading to recurrence of cerebral infarction and poor prognosis. Endovascular treatment can improve cerebral perfusion in patients with chronic symptomatic middle cerebral artery occlusion and reduce the risk of the recurrence of cerebral infarction，and it is an important treatment method for chronic symptomatic middle cerebral artery occlusion. However，ischemia-reperfusion injury is a common complication after endovascular treatment，which not only limits the efficacy of endovascular treatment but also seriously affects the prognosis of patients. Therefore，this article reviews the research advances in the onset mechanism of ischemia-reperfusion injury after endovascular treatment of chronic symptomatic middle cerebral artery occlusion and related intervention strategies，in order to provide a theoretical basis and treatment ideas for clinical practice.
Carnitine palmitoyltransferase Ⅱ （CPT Ⅱ） deficiency is an autosomal recessive disorder caused by mutations in the CPT2 gene，and it is characterized by impaired mitochondrial long-chain fatty acid β-oxidation and multi-organ energy metabolism dysfunction in the heart，liver，and skeletal muscle. The disease exhibits marked clinical heterogeneity，ranging from neonatal multi-organ failure to adult-onset myopathic forms induced by exercise，and its phenotypic variability is closely associated with mutation type，enzyme activity deficiency，and environmental triggers.Although neonatal screening techniques have improved diagnosis rate in asymptomatic individuals，limitations in acylcarnitine profiling，complex genotype-phenotype correlations，and diverse metabolic crises are still the factors leading to a high misdiagnosis rate in clinical practice. Supportive management is currently the main treatment method，with a lack of targeted therapies. This article systematically reviews the molecular mechanism，clinical subtypes，and diagnostic difficulties of CPT Ⅱ deficiency and discusses the treatment strategies based on precision medicine，in order to provide a basis for making decisions in clinical diagnosis and treatment and exploring the directions for the development of targeted therapies in the future.
Medical Publishing Centre of The First Hospital of Jilin University