The Impact of Lifestyle Factors on Migraine Frequency and Severity in Neurology

Objective: This systematic review examines the impact of lifestyle factors on migraine frequency and severity through a comprehensive analysis of lifestyle factors such as diet, physical activity, sleep patterns, stress, mental health, and environmental influences. Methods: We thoroughly searched Google Scholar, PUBMED, Scopus, and Web of Science databases using keywords related to migraines and lifestyle factors. Keywords incorporated the Boolean operator “and” to narrow search results. Following the PRISMA guidelines, we identified, screened, and evaluated studies for inclusion, resulting in nine studies meeting the eligibility criteria. Results: A total of 4917 records were initially identified from Scopus (2786), PubMed (854), and Web of Science (1277). Following deduplication, 3657 records underwent title screening, with 382 additionally screened by abstract. Ultimately, 88 full-text articles were assessed, resulting in 9 studies meeting eligibility for qualitative synthesis: 7 prospective and 2 retrospective studies. Our findings highlight the multifaceted role of lifestyle factors in migraine pathophysiology and management. Dietary habits, such as high-calorie, high-fat, and gluten-containing diets were linked to migraine triggers. Moderate physical activity showed beneficial effects on migraine management, while intense exercise could exacerbate symptoms. Poor sleep hygiene and insomnia were strongly associated with increased migraine frequency and severity. Chronic stress and poor mental health significantly contributed to migraine exacerbation, with stress management techniques proving beneficial. Environmental factors, including light, sound, weather changes, and allergens, were also identified as significant migraine triggers. Conclusions: Personalized lifestyle modifications, tailored to individual patient profiles, are crucial in managing migraines. Evidence-based recommendations include balanced diets, moderate physical activity, improved sleep hygiene, stress management techniques, and environmental adaptations.

Evaluation of the effectiveness of preventive nursing measures for pressure injuries in patients in the neurology intensive care unit

BACKGROUND Patients in neurology intensive care units(ICU)are prone to pressure injuries(PU)due to factors such as severe illness,long-term bed rest,and physiological dysfunction.PU not only causes pain and complications to patients,but also increases medical burden,prolongs hospitalization time,and affects the recovery process.AIM To evaluate and optimize the effectiveness of pressure injury prevention nursing measures in neurology ICU patients.METHODS A retrospective study was conducted,and 60 patients who were admitted to the ICU of the Department of Neurology were selected and divided into an observation group and a control group according to the order of admission,with 30 people in each group.The observation group implemented pressure injury prevention and nursing measures,while the control group adopted routine care.RESULTS Comparison between observation and control groups following pressure injury prevention nursing intervention revealed significantly lower incidence rates in the observation group compared to the control group at 48 h(8.3%vs 26.7%),7 d(16.7%vs 43.3%),and 14 d(20.0%vs 50.0%).This suggests a substantial reduction in pressure injury incidence in the observation group,with the gap widening over time.Additionally,patients in the observation group exhibited quicker recovery,with a shorter average time to get out of bed(48 h vs 72 h)and a shorter average length of stay(12 d vs 15 d)compared to the control group.Furthermore,post-intervention,patients in the observation group reported significantly improved quality of life scores,including higher scores in body satisfaction,feeling and function,and comfort(both psychological and physiological),indicating enhanced overall well-being and comfort following the implementation of pressure injury prevention nursing measures.CONCLUSION Implementing pressure injury preventive care measures for neurology ICU patients will have better results.

Potassium and calcium channels in different nerve cells act as therapeutic targets in neurological disorders

The central nervous system, information integration center of the body, is mainly composed of neurons and glial cells. The neuron is one of the most basic and important structural and functional units of the central nervous system, with sensory stimulation and excitation conduction functions. Astrocytes and microglia belong to the glial cell family, which is the main source of cytokines and represents the main defense system of the central nervous system. Nerve cells undergo neurotransmission or gliotransmission, which regulates neuronal activity via the ion channels, receptors, or transporters expressed on nerve cell membranes. Ion channels, composed of large transmembrane proteins, play crucial roles in maintaining nerve cell homeostasis. These channels are also important for control of the membrane potential and in the secretion of neurotransmitters. A variety of cellular functions and life activities, including functional regulation of the central nervous system, the generation and conduction of nerve excitation, the occurrence of receptor potential, heart pulsation, smooth muscle peristalsis, skeletal muscle contraction, and hormone secretion, are closely related to ion channels associated with passive transmembrane transport. Two types of ion channels in the central nervous system, potassium channels and calcium channels, are closely related to various neurological disorders, including Alzheimer's disease, Parkinson's disease, and epilepsy. Accordingly, various drugs that can affect these ion channels have been explored deeply to provide new directions for the treatment of these neurological disorders. In this review, we focus on the functions of potassium and calcium ion channels in different nerve cells and their involvement in neurological disorders such as Parkinson's disease, Alzheimer's disease, depression, epilepsy, autism, and rare disorders. We also describe several clinical drugs that target potassium or calcium channels in nerve cells and could be used to treat these disorders. We concluded that there are few clinical drugs that can improve the pathology these diseases by acting on potassium or calcium ions. Although a few novel ion-channelspecific modulators have been discovered, meaningful therapies have largely not yet been realized. The lack of target-specific drugs, their requirement to cross the blood–brain barrier, and their exact underlying mechanisms all need further attention. This review aims to explain the urgent problems that need research progress and provide comprehensive information aiming to arouse the research community's interest in the development of ion channel-targeting drugs and the identification of new therapeutic targets for that can increase the cure rate of nervous system diseases and reduce the occurrence of adverse reactions in other systems.

Exploiting fly models to investigate rare human neurological disorders

Rare neurological diseases,while individually are rare,collectively impact millions globally,leading to diverse and often severe neurological symptoms.Often attributed to genetic mutations that disrupt protein function or structure,understanding their genetic basis is crucial for accurate diagnosis and targeted therapies.To investigate the underlying pathogenesis of these conditions,researchers often use non-mammalian model organisms,such as Drosophila(fruit flies),which is valued for their genetic manipulability,cost-efficiency,and preservation of genes and biological functions across evolutionary time.Genetic tools available in Drosophila,including CRISPR-Cas9,offer a means to manipulate gene expression,allowing for a deep exploration of the genetic underpinnings of rare neurological diseases.Drosophila boasts a versatile genetic toolkit,rapid generation turnover,and ease of large-scale experimentation,making it an invaluable resource for identifying potential drug candidates.Researchers can expose flies carrying disease-associated mutations to various compounds,rapidly pinpointing promising therapeutic agents for further investigation in mammalian models and,ultimately,clinical trials.In this comprehensive review,we explore rare neurological diseases where fly research has significantly contributed to our understanding of their genetic basis,pathophysiology,and potential therapeutic implications.We discuss rare diseases associated with both neuron-expressed and glial-expressed genes.Specific cases include mutations in CDK19 resulting in epilepsy and developmental delay,mutations in TIAM1 leading to a neurodevelopmental disorder with seizures and language delay,and mutations in IRF2BPL causing seizures,a neurodevelopmental disorder with regression,loss of speech,and abnormal movements.And we explore mutations in EMC1 related to cerebellar atrophy,visual impairment,psychomotor retardation,and gain-of-function mutations in ACOX1 causing Mitchell syndrome.Loss-of-function mutations in ACOX1 result in ACOX1 deficiency,characterized by very-long-chain fatty acid accumulation and glial degeneration.Notably,this review highlights how modeling these diseases in Drosophila has provided valuable insights into their pathophysiology,offering a platform for the rapid identification of potential therapeutic interventions.Rare neurological diseases involve a wide range of expression systems,and sometimes common phenotypes can be found among different genes that cause abnormalities in neurons or glia.Furthermore,mutations within the same gene may result in varying functional outcomes,such as complete loss of function,partial loss of function,or gain-of-function mutations.The phenotypes observed in patients can differ significantly,underscoring the complexity of these conditions.In conclusion,Drosophila represents an indispensable and cost-effective tool for investigating rare neurological diseases.By facilitating the modeling of these conditions,Drosophila contributes to a deeper understanding of their genetic basis,pathophysiology,and potential therapies.This approach accelerates the discovery of promising drug candidates,ultimately benefiting patients affected by these complex and understudied diseases.

Targeting capabilities of engineered extracellular vesicles for the treatment of neurological diseases

Recent advances in research on extracellular vesicles have significantly enhanced their potential as therapeutic agents for neurological diseases.Owing to their therapeutic properties and ability to cross the blood–brain barrier,extracellular vesicles are recognized as promising drug delivery vehicles for various neurological conditions,including ischemic stroke,traumatic brain injury,neurodegenerative diseases,glioma,and psychosis.However,the clinical application of natural extracellular vesicles is hindered by their limited targeting ability and short clearance from the body.To address these limitations,multiple engineering strategies have been developed to enhance the targeting capabilities of extracellular vesicles,thereby enabling the delivery of therapeutic contents to specific tissues or cells.Therefore,this review aims to highlight the latest advancements in natural and targeting-engineered extracellular vesicles,exploring their applications in treating traumatic brain injury,ischemic stroke,Parkinson's disease,Alzheimer's disease,amyotrophic lateral sclerosis,glioma,and psychosis.Additionally,we summarized recent clinical trials involving extracellular vesicles and discussed the challenges and future prospects of using targeting-engineered extracellular vesicles for drug delivery in treating neurological diseases.This review offers new insights for developing highly targeted therapies in this field.

Neurology:颈动脉蹼——缺血性卒中新的危险因素

颈动脉蹼（carotid web）是位于颈动脉球后壁颈动脉分叉以远的腔内薄层突出物。有人认为它是肌纤维发育不良的一种少见表现形式,也有人认为它是一种发育异常,容易被误诊为动脉粥样硬化斑块。颈动脉蹼在计算机断层扫描血管造影（computed tomography angiography,CTA）矢状切位表现为颈动脉分叉以远,沿着颈动脉后壁向腔内伸展的薄层充盈缺损;轴位表现为薄层隔膜。

Neurology:眶梗死综合征1例

2016年,David Dongkyung Kim在Neurosurgery上发表了一篇眶梗死综合征（orbital infarction syndrome）的病例报告。

Neurology:应该拒绝痴呆患者静脉溶栓吗?

痴呆不是急性缺血性卒中溶栓的禁忌证,但是大部分溶栓研究都把80岁或90岁以上患者排除在外,当前溶栓指南对这些患者的推荐意见存在差异。按照美国心脏学会（American Heart Association,AHA）/美国卒中学会（American Stroke Association,ASA）指南推荐,痴呆患者也可以从静脉溶栓中获益,然而制定决策前应该考虑患者发病前的功能状态。

Neurology：血小板计数100×10^9/L作为静脉溶栓的阈值受到挑战

静脉溶栓是治疗急性缺血性卒中有效和安全的方法,患者越早治疗预后越好,但血小板计数（platelet count,PC）对患者预后（包括出血的风险、功能预后及死亡）的影响尚不清楚。按照目前美国和欧洲指南,PC〈100×10^9/L是静脉溶栓的禁忌证。但是,这个阈值仅基于专家意见,因此还需要进一步研究证实。同时美国指南认为获得PC结果前就可以开始静脉溶栓,但欧洲指南并未推荐。

Neurology:两例少见原因弥漫性脑微出血

病例1：患者男性,61岁。抵达阿塔卡玛（海拔4000米）2 d后出现霹雳样头痛,随后意识丧失。转运到低海拔地区后病情逐渐好转。头颅磁共振成像（magnetic resonance imaging,MRI）显示弥漫性血管源性水肿和微出血（图1）。最终诊断为高海拔脑水肿。病例2：患者男,51岁。因为吸入性肺炎、缺氧和急性呼吸窘迫综合征住院。抗生素治疗后病情改善,1周后痫性发作。脑MRI显示弥漫性脑微出血（图2）。

Neurology：弥散加权成像阳性小病灶在脑小血管病发生发展过程中的作用

脑小血管病(small vessel disease,SVD)是导致痴呆的最重要的血管性因素。SVD的MRI标志物包括脑白质高信号(white matter hyperintensities,WMH)、腔隙和微出血等。通常认为慢性低灌注在SVD的病因学中扮演着重要角色,尽管从未被纵向研究证明。

Neurology:假瘤样脑淀粉样血管病相关炎症反应

脑淀粉样血管病（cerebral amyloid angiopathy,CAA）是常见的脑小血管病,特征为大脑皮层和软脑膜的小到中等粗细动脉、小动脉和毛细血管等血管壁β淀粉样蛋白（amyloid β-protein,Aβ）逐渐沉积。脑叶出血是CAA典型的临床表现,还可以表现为认知功能下降,痴呆,以及短暂性神经系统症状。

Neuronal injury and brain-derived neurotrophic factor expression in a rat model of amygdala kindling seizures Differences in brain regions and kindling courses

BACKGROUND：Studies have demonstrated that brain-derived neurotrophic factor （BDNF） has a dual effect on epilepsy. However, the relationship between epilepsy-induced brain injury and BDNF remains poorly understood.OBJECTIVE：According to ultrastructural and molecular parameters, to detect the degree of neuronal injury and BDNF expression changes at different brain regions and different kindling times to determine the effects of BDNF on epilepsy-induced brain injury.DESIGN, TIME AND SETTING：A randomized, controlled, animal experiment based on neuropathology and molecular biology was performed at the Department of Physiology and Department of Pathology, Basic Medical College of Jilin University in 2003.MATERIALS：UltraSensitiveTM SP kit for immunohistochemistry （Fuzhou Maxim Biotechnology, China）, BDNF antibody （concentrated type, Wuhan Boster Biological Technology, China）, JEM-1000SX transmission electron microscopy （JEOL, Japan）, and BH-2 light microscope （Olympus, Japan） were used in the present study.METHODS：Wistar rats were randomly assigned to control （n = 6）, sham-surgery （n = 6）, and model （n = 60） groups. The control group rats were not treated; an electrode was embedded into the amygdala in rats from the sham-surgery and model groups; an amygdala kindling epilepsy model was established in the model group.MAIN OUTCOME MEASURES：Pathological changes in the temporal lobe and hippocampus were observed by light and electron microscopy at 1, 3, 7, 14, and 21 days following kindling, and BDNF expression in the various brain regions was determined by immunohistochemistry.RESULTS：In the model group, temporal lobe cortical and hippocampal neurons were swollen and the nuclei were laterally deviated. There were also some apoptotic neurons 3 days after kindling. The nucleoli disappeared and the nuclei appeared broken or lysed, as well as slight microglia hyperplasia, at 7 days. Electron microscopic observation displayed chromatin aggregation in the nuclei and slight mitochondrion swelling 3 days after kindling. Injury changes were aggravated at 7 days, characterized by broken cytoplasmic membrane and pyknosis. With the development of seizure, the number of BDNF-positive neurons in the hippocampus and temporal lobe increased and peaked at 7 days. Moreover, hippocampal and cortical temporal lobe injury continued. Following termination of electrical stimulation after 7 days of kindling, BDNF expression decreased, but continued to be expressed, up to 21 days of kindling. In addition, the number of temporal and hippocampal BDNF-positive neurons was greater than the control group.CONCLUSION：Brain injury and BDNF expression peaked at 7 days after kindling, and hippocampal changes were significant.

Effect of Adenosine A2A Receptor Antagonist ZM241385 on Amygdala-kindled Seizures and Progression of Amygdala Kindling

The purpose of this study was to evaluate the effect of adenosine A2A receptor antagonist ZM241385 on amygdala-kindled seizures and its roles in epileptogenesis. Electrodes were implanted into the right amygdala of male adult Wistar rats. Kindling was accomplished by using stimulus strength of 500 μA applied daily to the amygdala until 10 consecutive stage 5 seizues were induced. Then effect of ZM241385 was studied in fully kindled rats after intracerebroventricular administration of the drug. In addition, the effect on kindling progression was evaluated through ZM241385 injection before daily stimulation. In all experiments, behavioral changes in the rats in response to ZM241385 were monitored closely. The results showed that, in fully amygdala-kindled rats, ZM241385 (0.001–0.1 nmol/L) decreased afterdischage duration (ADD), motor seizure duration (MSD), stage 5 duration (S5D) and seizure duration (SD), but only the effect on ADD was dose-dependent. The doses of 0.001–0.1 nmol/L had no influence on stage 4 latency (S4L) and seizure stage (SS). The dosages of 0.0001 and 1 nmol/L of ZM241385 did not exert any effect on all seizure parameters. In contrast to the results in fully amygdala-kindled rats, ZM241385 (0.001–0.1 nmol/L) had minimal or no effects on the progression of amygdala-kindled seizures. We are led to the conclusion that although ZM241385 had no influence on the progression of amygdala-kindled seizures, it had potent anticonvulsant profile and little adverse effects at the dosage of 0.001–0.1 nmol/L, suggesting that the agent is effective against the amygdala-kindled seizures.

Characteristic Duties of Critical Care Nurses in Japan: A Time-Study Comparison with Neurology Ward Nurses

Background: The importance of the acute phase in hospitals has been increasing. While administering high-level critical care, the working styles of critical care nurses, the types of clinical care they provide, and the way in which they prioritize tasks, remain unclear. Aim of this study was to elucidate the characteristic duties of critical care nurses through a comparison with neurological ward nurses. Methods: We recorded the duties of critical care nurses and neurology ward nurses (10 each) using a time-study design. Duties were measured separately by action, classified using a classification table, and differences between the two groups were compared. Results: No differences in the number of actions were observed between the two groups. The top five items that required the most time for critical care nurses were, “Movement”, “Administration and oxygen management”, “Handover process/Doctor’s rounds”, “Preparation for entry and exit management of patients”, and “Bed bathing (for bedbound patients)”. Of the 195 items, significant differences between the groups were noted for 34 items, while the duties of critical care nurses were best characterized by bed bathing (for bedbound patients), changing position, confirmation of infusion tubes, handover process/doctor’s rounds, and preparation for entry and exit management of patients. Conclusion: A characteristic of critical care nurses is that they must remain near patients and perform tasks while moving only a short distance. Moreover, the promotion of tasks while communicating with physicians is presumed to play a role in the promotion of team medicine. Furthermore, much time was spent caring for patients in bed, and a lot of time was devoted to the preparation and finalizing of treatments and care, suggesting the possibility that more time can be spent on caring for patients through a revision of duties.

Psychological Influence Factors Analysis of the New Generation Employees’ Moral Choices from the Perspective of Cognitive Neurology

At present,the academic researches on moral choices focus mainly on the individuals’external behaviors,without fully considering the influences of the individuals’internal psychological factors.Based on the model of complete information static games in the Non-cooperative Game theory,the present research has designed a“Red and Blue Experiment”to explore the psychological influencing factors of the new generation employees’moral choices.The research has conducted psychoanalysis on the new generation employees through experiments and interviews with 118 data sources,and concluded the characteristics in relation to the different stages of psychological processes and moral choices of the experimental population.Through comparative analysis,it is found that:the psychological factors,such as trust,doubt,and guilt will influence the new generation employees’moral choices,guiding them to make choices,such as risk aversion and mutual benefit and win-win,in the process.Additionally,the research has also provided effective scientific evidence for the new generation employees’mental health development and career planning.

Kdm6a-CNN1 axis orchestrates epigenetic control of traumainduced spinal cord microvascular endothelial cell senescence to balance neuroinflammation for improved neurological repair

Cellular senescence assumes pivotal roles in various diseases through the secretion of proinflammatory factors.Despite extensive investigations into vascular senescence associated with aging and degenerative diseases,the molecular mechanisms governing microvascular endothelial cell senescence induced by traumatic stress,particularly its involvement in senescence-induced inflammation,remain insufficiently elucidated.In this study,we present a comprehensive demonstration and characterization of microvascular endothelial cell senescence induced by spinal cord injury(SCI).Lysine demethylase 6A(Kdm6a),commonly known as UTX,emerges as a crucial regulator of cell senescence in injured spinal cord microvascular endothelial cells(SCMECs).Upregulation of UTX induces senescence in SCMECs,leading to an amplified release of proinflammatory factors,specifically the senescenceassociated secretory phenotype(SASP)components,thereby modulating the inflammatory microenvironment.Conversely,the deletion of UTX in endothelial cells shields SCMECs against senescence,mitigates the release of proinflammatory SASP factors,and promotes neurological functional recovery after SCI.UTX forms an epigenetic regulatory axis by binding to calponin 1(CNN1),orchestrating trauma-induced SCMECs senescence and SASP secretion,thereby influencing neuroinflammation and neurological functional repair.Furthermore,local delivery of a senolytic drug reduces senescent SCMECs and suppresses proinflammatory SASP secretion,reinstating a local regenerative microenvironment and enhancing functional repair after SCI.In conclusion,targeting the UTX-CNN1 epigenetic axis to prevent trauma-induced SCMECs senescence holds the potential to inhibit SASP secretion,alleviate neuroinflammation,and provide a novel treatment strategy for SCI repair.

Meta-analyses in the wonderl and of neurology

Meta-analyses are often misused and underused in neurology. This editorial provides some comments on the role of meta-analyses in neurological research.Recently, a huge increase in the number of metaanalyses and systematic reviews has been observed in neurological journals. The major strengths of metaanalyses are the increase of statistical power. However, as for any other investigative tool, meta-analytic research is a research method itself which can produce severe shortcomings. Specifically, the issues of search terms, time periods of published studies, databases used for searching, the definitions of inclusion and exclusion criteria for papers(which greatly affect clinical heterogeneity), publication bias; and the statistical methods used, dramatically influence the results of metaanalyses. The main problem of meta-analyses is that they cannot be expected to overcome the limitations of the studies they include(the so-called "garbage in,garbage out" phenomenon). Furthermore, most systematic reviews in the neurological literature lead to the unsatisfying and clinically frustrating statement "further studies are needed". However it is much more frustrating to see how the gaps in scientific knowledge identified by meta-analyses have not been translated into serious efforts to fill them. Besides their role in evaluating efficacy and tolerability of drugs, meta-analyses may be used to assess diagnostic values of debatable clinical findings, as they represent powerful tools to try to answer questions not posed by individual studies and to settle controversies arising from conflicting claims.

Hippocampal High-Frequency Stimulation Inhibites the Progression of Rapid Kindling-Induced Seizure in Rats

Epilepsy is one of the most common serious neurological disorders. Pharmacoresistant epilepsy patients are poorly controlled or their seizures are refractory to drug treatment. Resective surgery is frequently a promising therapy in this population, however, not all the patients meet the eligibility criteria for the surgical treatment. Deep brain stimulation has been investigated in clinical studies and animal studies as an alternative treatment, but the optimal stimulation parameters remain an issue. The present study was designed to investigate the effect of unilateral high-frequency stimulation (HFS) of hippocampus on seizure development by using the hippocampal rapid kindling method (hRK) in rats, and compared the results with those of low-frequency stimulation previously published by our group. We used male Wistar rats implanted with electrodes in the ventral hippocampus. All rats underwent hRK (biphasic square wave pulses, 20 Hz for 10 seconds) during three consecutive days (twelve stimulations per day). The control group (hRK;n = 7) received only RK stimulus, while the treated group (HFS-hRK;n = 9) received also HFS (biphasic square wave pulses, 130 Hz for 30 seconds) immediately before the RK stimulus, during three consecutive days. At the end of behavioral testing 78% (p 0.01) of the animals receiving HFS treatment were still not fully kindled staying in stages 0 -III (p 0.01). HFS group needed a higher number of stimulations to achieve stage III (p 0.05) with respect to control group. However, no significant differences in the cumulative daily afterdischarge duration were observed. HFS did not present significant differences compared with LFS in any of studied parameters. The findings suggest that unilateral HFS applied on hippocampus effectively inhibited the epileptogenic process induced by hippocampal rapid kindling. According to the comparative results about hippocampal rapid kindled animals stimulated with HFS and LFS (5 Hz), we found no conclusive information on which treatment is most efficient.