Cognitive impairment in cerebral small vessel disease induced by hypertension

Hypertension is a primary risk factor for the progression of cognitive impairment caused by cerebral small vessel disease,the most common cerebrovascular disease.Howeve r,the causal relationship between hypertension and cerebral small vessel disease remains unclear.Hypertension has substantial negative impacts on brain health and is recognized as a risk factor for cerebrovascular disease.Chronic hypertension and lifestyle factors are associated with risks for stro ke and dementia,and cerebral small vessel disease can cause dementia and stroke.Hypertension is the main driver of cerebral small vessel disease,which changes the structure and function of cerebral vessels via various mechanisms and leads to lacunar infarction,leukoaraiosis,white matter lesions,and intracerebral hemorrhage,ultimately res ulting in cognitive decline and demonstrating that the brain is the to rget organ of hypertension.This review updates our understanding of the pathogenesis of hypertensioninduced cerebral small vessel disease and the res ulting changes in brain structure and function and declines in cognitive ability.We also discuss drugs to treat cerebral small vessel disease and cognitive impairment.

Correlating cognitive impairment with carotid atherosclerosis and carotid artery stenosis in patients with acute cerebral infarction

BACKGROUND：Studies have demonstrated that carotid atherosclerosis and carotid artery stenosis are closely associated with cognitive impairment in patients with and without clinically evident cerebrovascular disease. OBJECTIVE： To investigate the correlation between the degree of pathological changes in carotid atherosclerosis, carotid artery stenosis, and cognitive impairment in patients with acute cerebral infarction through the use of color Doppler imaging. DESIGN, TIME AND SETTING： The present concurrent, non-randomized, controlled experiment was performed at the Departments of Neurology and Ultrasound, Affiliated Hospital of North Sichuan Medical College between November 2006 and August 2007. PARTICIPANTS： Fifty-five patients with cerebral infarction, consisting of 35 males and 20 females, aged 50–82 years, were admitted to the hospital between November 2006 and August 2007 and recruited for this study. An additional 30 subjects consisting of 18 males and 12 females, aged 47–78 years, that concurrently received a health examination at the same hospital, were also included as normal controls. METHODS： Intima-media thickness （IMT）, plaque shape, size, and echo intensity of all subjects were detected by color Doppler flow imaging. Assessment criteria： IMT 〉 1.0 mm was considered to be intimal thickening, and IMT 〉 1.2 mm was determined to be formed atherosclerotic plaques. In the position of the largest plaque, the degree of carotid artery stenosis was determined by the following formula： （1-cross-sectional area of residual vascular luminal area/vascular cross-sectional area） × 100%. Less than 30% exhibited mild stenosis, 30%-40% moderate stenosis, and 〉 50% severe stenosis. MAIN OUTCOME MEASURES： IMT and the degree of carotid artery stenosis were evaluated by color Doppler flow imaging. The Mini-Mental State Examination （MMSE）, as well as the clinical memory scale, was compared between patients with cerebral infarction and normal controls. RESULTS： In the cerebral infarction group, IMT was increased, the degree of carotid artery stenosis was aggravated, and the MMSE and MQ scores of clinical memory scale were decreased. In particular, orientation of time and place, attention, calculation, and short-time memory were decreased. There were statistically significant differences in MMSE and MQ of clinical memory scale between patients with cerebral infarction and normal controls （P 〈 0.01）. The scores from the two scales were significantly lower in patients with cerebral infarction with carotid plaque subgroup compared to the cerebral infarction with no carotid plaque subgroup （P 〈 0.01）. The scores from the two scales were also significantly lower in patients with IMT 〉 1.0 mm, as well as moderate and severe carotid artery stenosis, compared to patients with IMT ≤ 1.0 mm, and normal and mild stenosis group （P 〈 0.05）. CONCLUSION： More severe atherosclerotic and carotid artery stenosis leads to more obvious cognitive impairment.

Effects of Yinxingdamo Injection Combined with Oxiracetam Capsule on Cognitive Function and Neurological Deficit in Patients with Acute Cerebral Infarction

OBJETTIVE: To observe the effects of Yinxingdamo Injection combined with oxiracetam capsule on cognitive function and neurological deficit in patients with acute cerebral infarction. METHODS: A total of 76 patients with acute cerebral infarction were randomly divided into observation group and control group, with 38 patients in each group. Patients in the control group were treated with conventional western medicine and oxiracetam capsules while patients in the observation group were given Yinxingdamo injection intravenous drip treatment on the basis of the same treatment. After 4 weeks of treatment, the cognitive function of the two groups before and after treatment was observed [Simple Intelligence Scale(MMSE Score), Montreal Cognitive Assessment Scale(MoCA Score)], Neurological Deficit [Chinese Stroke Scale(CSS Score), Daily Life Activity ability(ADL score)], free radical biochemical indicators [malondialdehyde(MDA), oxide dismutase(SOD)] changes, and statistical effects of two groups. RESULTS: After treatment, the total effective rate of the observation group was 92.1%, which was significantly higher than 73.7% of the control group(P < 0.05). The MMSE score and MoCA score of the two groups were significantly increased after treatment(P < 0.05), and the MMSE score and MoCA score inobservation group were significantly increased after treatment than the control group(P < 0.05). The CSS scores of the two groups were significantly decreased after treatment(P < 0.05), and the ADL scores were significantly increased(P < 0.05). The improvement of CSS score and ADL score in the observation group were significantly better than those in the control group(P < 0.05), and serum MDA levels were significantly decreased in both groups after treatment(P < 0.05), and SOD levels were significantly increased(P < 0.05), and the improvement of MDA and SOD levels in the observation group was significantly better than that in the control group group(P < 0.05). CONCLUSION: Yinxingdamo injection combined with oxiracetam capsule can effectively inhibit the oxygen free radical reaction injury in patients with acute cerebral infarction, and significantly improve the symptoms of cognitive dysfunction and neurological deficit in patients. Its curative effect is exact and worthy of clinical application.

The clinical and experimental study of the efficacy of nimodiping in cognitive rehabilitation of cerebral infarction

Objective To study the efficacy of nimodipine in cognitive rehabilitation of the cerebral infarction.Method (1)Experimental animal models were created in 24 month old Wistar rats,which were treated with nimodipine.Results were compared among the drug treated group,non treated of the same age mice group and 8 month old mice group.(2)Clinical research of nimodipine was conducted in 67 cerebral infarction patients with cognitive impairments.HDS was used as measuring tool.(3)To analyze the related factors such as age,Barthel index and FAQ.Result After 1 month treatment of nimodipine,significant differences between drug dealing and non drug dealing groups were showed in the Y maze discrimination learning experiment(P< 0.05),the duration and errors were improved in drug treated group compared with control group.No significant different result was found in one trial passive avoidance response experiment(P >0.05);single factor analysis(including Barthel index,FAQ and age) did not show significance(P >0.05);there is no statistical differences between nimodipine treated patients and non drug treatment patients(P >0.05).Conclusion Nimodipine showed no efficacy to cognitive rehabilitation in cerebral infarctions.

Effects of angiotensin converting enzyme inhibitors on cognitive function, apoptosis and oxidative stress in brain tissue of rats with cerebral infarction

Objective:To study the effects of angiotensin converting enzyme inhibitor(ACEI)on cognitive function,apoptosis and oxidative stress in brain tissue of rats with cerebral infarction.Methods:Adult male SD rats were randomly divided into control group,cerebral infarction group and ACEI group.The latter two groups were used to establish cerebral infarction model by thread embolism.The ACEI group was given oral administration of fosinopril 10mg/kg,and the other two groups were given oral administration of saline.The differences of Morris water maze cognitive function,apoptotic genes and oxidative stress indexes were compared among the three groups.Results:The escape latency of rats in cerebral infarction group was significantly longer than that in control group,the number of times of platform crossing was significantly less than that in control group,the duration of platform stay was significantly shorter than that in control group,the mRNA expression levels of Bcl-2 associated X protein(Bax),factor associated suicide(Fas),Fas ligand(FasL)and Caspase-3,the protein expression levels of phosphorylated Janus kinase(p-JAK2)and phosphorylated signal transducer and activator of transcription(p-STAT3)as well as the contents of reactive oxygen species(ROS)and malonaldehyde(MDA)in brain tissue were significantly higher than those in control group,and the mRNA expression level of B-cell lymphoma-2(Bcl-2)as well as the contents of catalase(CAT)and superoxide dismutase(SOD)in brain tissue was significantly lower than those in control group.The escape latency of rats in ACEI group was significantly shorter than that in cerebral infarction group,the number of times of platform crossing was significantly more than that in cerebral infarction group,the duration of platform stay was significantly longer than that in cerebral infarction group,the mRNA expression levels of Bax,Fas,FasL and Caspase-3,the protein expression levels of p-JAK2 and p-STAT3 as well as the contents of ROS and MDA in brain tissue were significantly lower than those in cerebral infarction group,and the mRNA expression level of Bcl-2 as well as the contents of CAT and SOD in brain tissue was significantly higher than those in cerebral infarction group.Conclusions:ACEI can improve the cognitive function of rats with cerebral infarction and inhibit the apoptosis and oxidative stress in ischemic brain tissue.

Changes of auditory evoked magnetic fields in patients after acute cerebral infarction using magnetoencephalography

Auditory evoked magnetic fields were recorded from 15 patients with acute cerebral infarction and 11 healthy volunteers using magnetoencephalography.The auditory stimuli of 2 kHz pure tone were binaurally presented with an interstimulus interval of 1 second.The intensity of stimuli was 90 dB and the stimulus duration was 8 ms.The results showed that the M100 was the prominent response, peaking approximately 100 ms after stimulus onset in all subjects.It originated from the area close to Heschl’s gyrus.In the patient group,the peak latency of M100 responses was significantly prolonged,and the mean strength of equivalent current dipole was significantly smaller in the affected hemisphere.The three-dimensional inter-hemispheric difference of the M100 positions was increased in the patient group.Our experimental findings suggested that impairment of cerebral function in patients with acute ischemic stroke can be detected using magnetoencephalography with the higher spatial resolution and temporal resolution.Magnetoencephalography could provide objective and sensitive indices to estimate auditory cortex function in patients with acute cerebral infarction.

Significance of neuroglobin in serum of acute atherosclerotic cerebral infarction patients

This study sought to examine neuroglobin （NGB） in the serum of acute cerebral infarction patients with double-antibody sandwich enzyme-linked immunosorbent assay to identify all risk factors, calculate infarct size, assess neurological impairment, and analyze the relation between NGB and each of these factors. The double-antibody sandwich assay indicated that levels of NGB in serum were unaltered within 6 hours following acute cerebral infarction compared with normal levels. NGB levels then underwent a distinct change, peaking at 24 hours then returning to normal levels in 72 hours. The results suggest that the level of NGB might be related to infarct size and low-density lipoprotein at 24 hours after acute cerebral infarction. There were no significant differences in neurological impairment scores and infarct size at different periods following infarction. The findings indicated that the level of NGB in serum of acute cerebral infarction patients was correlated with infarct time.

β2-Microglobulin exacerbates neuroinflammation,brain damage,and cognitive impairment after stroke in rats

β2-Microglobulin(β2M),a component of the major histocompatibility complex class I molecule,is associated with aging-related cognitive impairment and Alzheimer’s disease.Although upregulation ofβ2M is considered to be highly related to ischemic stroke,the specific role and underlying mechanistic action ofβ2M are poorly understood.In this study,we established a rat model of focal cerebral ischemia by occlusion of the middle cerebral artery.We found thatβ2M levels in the cerebral spinal fluid,serum,and brain tissue were significantly increased in the acute period but gradually decreased during the recovery period.RNA interference was used to inhibitβ2M expression in the acute period of cerebral stroke.Tissue staining with 2,3,5-triphenyltetrazolium chloride and evaluation of cognitive function using the Morris water maze test demonstrated that decreasedβ2M expression in the ischemic penumbra reduced infarct volume and alleviated cognitive deficits,respectively.Notably,glial cell,caspase-1(p20),and Nod-like receptor pyrin domain containing 3(NLRP3)inflammasome activation as well as production of the inflammatory cytokines interleukin-1β,interleukin-6,and tumor necrosis factor-αwere also effectively inhibited byβ2M silencing.These findings suggest thatβ2M participates in brain injury and cognitive impairment in a rat model of ischemic stroke through activation of neuroinflammation associated with the NLRP3 inflammasome.

Offspring of rats with cerebral hypoxia-ischemia manifest cognitive dysfunction in learning and memory abilities

Neonatal hypoxic-ischemic encephalopathy is a serious neurological disease,often resulting in long-term neurodevelopmental disorders among surviving children.However,whether these neurodevelopmental issues can be passed to offspring remains unclear.The right common carotid artery of 7-day-old parental-generation rats was subjected to permanent ligation using a vessel electrocoagulator.Neonatal hypoxic-ischemic rat models were established by subjecting the rats to 8%O2–92%N2 for 2 hours.The results showed that 24 hours after hypoxia and ischemia,pathological damage,cerebral atrophy,liquefaction,and impairment were found,and Zea-Longa scores were significantly increased.The parental-generation rats were propagated at 3 months old,and offspring were obtained.No changes in the overall brain structures of these offspring rats were identified by magnetic resonance imaging.However,the escape latency was longer and the number of platform crossings was reduced among these offspring compared with normal rats.These results indicated that the offspring of hypoxic-ischemic encephalopathy model rats displayed cognitive impairments in learning and memory.This study was approved by the Animal Care&Welfare Committee of Kunming Medical University,China in 2018(approval No.kmmu2019072).

Microbleeds in fronto-subcortical circuits are predictive of dementia conversion in patients with vascular cognitive impairment but no dementia

Cerebral small vessel disease（CSVD） is a common etiology of vascular cognitive impairment with no dementia（V-CIND）. Studies have revealed that cerebral microbleeds（CMBs）, a feature of CSVD, contribute to cognitive impairment. However, the association between CMBs and dementia conversion in individuals with V-CIND is still unclear. Here, we analyzed the predictive role of CMBs in the conversion from V-CIND to dementia in CSVD patients. We recruited and prospectively assessed 85 patients with CSVD and V-CIND. V-CIND was evaluated using a series of comprehensive neuropsychological scales, including the Chinese version of the Montreal Cognitive Assessment and the Clinical Dementia Rating. MRI assessments were used to quantify lacunar infarcts, white matter hyperintensities, CMBs, and medial temporal lobe atrophy. Eighty-two of the 85 patients completed the assessment for dementia conversion at a 1-year follow-up assessment. Multivariate logistic regression analyses were conducted to examine independent clinical and MRI variables associated with dementia conversion. Twenty-four patients（29.3%） had converted to dementia at the 1-year follow-up, and these individuals had significantly more CMBs in the fronto-subcortical circuits. Multivariate logistic regression analyses revealed that the patients with CMBs in the fronto-subcortical circuits（odds ratio = 4.4; 95% confidence interval： 1.602-12.081, P = 0.004） and 5 or more CMBs overall（odds ratio = 17.6, 95% confidence interval： 3.23-95.84, P = 0.001） had a significantly increased risk of dementia at the 1-year follow-up. These findings indicate that CMBs in the fronto-subcortical circuits may be predictive of dementia conversion in CSVD patients with V-CIND, and thus extend the clinical significance of CMBs.

Cerebrovascular hemodynamics in patients with cerebral arteriosclerosis

The present study observed hemodynamic changes in 26 patients with cerebral arteriosclerosis using a cerebral circulation dynamics detector and transcranial Doppler. In patients with cerebral arteriosclerosis the blood supply and flow rate in the bilateral carotid arteries and the blood flow rate in the anterior cerebral and middle cerebral arteries were similar to normal controls, but the cerebral vascular resistance, critical pressure and pulsatility index were increased, and cerebral arterial elasticity and cerebral blood flow autoregulation were decreased. Compared with the lesioned hemisphere of patients with cerebral infarction, the total blood supply and blood flow rate of patients with cerebral arteriosclerosis were higher. Compared with normal subjects, patients with cerebral arteriosclerosis exhibited cognitive disturbances, mainly in short-term memory, attention, abstract capability, and spatial and executive dysfunction. Results showed that cerebral arteriosclerosis does not directly affect the blood supply of a cerebral hemisphere, but affects cognitive function. The increased cerebral vascular resistance and reduced autoregulation of cerebral blood vessels may be important hemodynamic mechanisms of arteriosclerosis-induced cerebral infarction.

醒脑开窍针刺法联合中药治疗脑梗死后轻度认知障碍的疗效观察

目的 观察醒脑开窍针刺法联合补肾益髓汤治疗脑梗死后轻度认知障碍的临床疗效。方法 将80例脑梗死后轻度认知障碍的患者随机分为研究组(40例)和对照组(40例)。两组均予基础治疗,研究组在基础治疗外另予醒脑开窍针刺法联合补肾益髓汤治疗。比较两组临床疗效,观察两组治疗前后简易精神状态检查表(mini-mental state examination,MMSE)、蒙特利尔认知评估(Montreal cognitive assessment,MoCA)和Rivermead行为记忆测验(Rivermead behavioural memory test,RBMT)的评分变化,观察两组治疗前后连线测验-B(trail making test-B,TMT-B)结果、血清淀粉样蛋白A(serum amyloid A,SAA)和β-淀粉样蛋白(amyloid β-protein,Aβ)水平以及脑微循环指标(颈总动脉的平均血流量、最大血流速度、最小血流速度、临界压力、脉搏速度、特性阻抗、外周阻力和动态阻力)的变化。结果 研究组总有效率高于对照组(P<0.05)。治疗后,两组MMSE、MoCA和RBMT评分均高于同组治疗前(P<0.05),且研究组上述评分均高于对照组(P<0.05)。治疗后,两组TMT-B结果以及SAA和Aβ水平均优于同组治疗前(P<0.05),且研究组上述指标优于对照组(P<0.05)。治疗后,两组脑微循环指标均较治疗前改善(P<0.05),且研究组优于对照组(P<0.05)。结论 在基础治疗以上,采用醒脑开窍针刺法联合补肾益髓汤治疗脑梗死后轻度认知障碍可提高临床疗效,能进一步改善患者认知功能,并调节SAA和Aβ水平。

血清小而密低密度脂蛋白胆固醇和总抗氧化能力水平与脑梗死患者认知功能障碍的相关性分析

目的:探究脑梗死患者血清小而密低密度脂蛋白胆固醇(small dense low-density lipoprotein cholesterol, sdLDL-C)和总抗氧化能力(total antioxidant capacity, T-AOC)水平变化及其与认知功能障碍发生的关系。方法:选择148例脑梗死患者,依据发病后7 d是否出现认知功能障碍,分为非障碍组(n=77)和障碍组(n=71);分别采用过氧化氢酶法和比色法测定两组血清sdLDL-C和T-AOC水平,并进行比较;Pearson相关系数法分析脑梗死患者血清sdLDL-C、T-AOC水平与蒙特利尔认知评估(MoCA)评分相关性;二元Logistic回归分析影响脑梗死患者认知功能障碍发生的危险因素。结果:与非障碍组相比,障碍组血清sdLDL-C水平明显升高(P<0.05),T-AOC水平明显降低(P<0.05)。相关性分析显示,血清sdLDL-C水平与MoCA评分呈负相关(r=-0.516,P<0.05),T-AOC水平与MoCA评分呈正相关(r=0.446,P<0.05)。Logistic回归分析显示,高血压、糖尿病、病情严重程度、血清sdLDL-C和T-AOC是脑梗死患者认知功能障碍发生的独立影响因素(P<0.05)。结论:脑梗死患者血清sdLDL-C水平升高,T-AOC水平降低,二者是影响脑梗死患者并发认知功能障碍的独立影响因素。

交叉性小脑神经机能联系不能1例报道并文献复习

交叉性小脑神经机能联系不能(crossed cerebellar diaschisis,CCD)是指当一侧大脑半球发生病变时,病灶对侧小脑半球出现血流量减少、葡萄糖氧化代谢水平下降的功能障碍,严重时甚至可能出现交叉性小脑萎缩的现象。CCD在临床工作中易被忽略或误诊。本文报告1例因左侧幕上脑梗死出现CCD导致左侧肢体共济失调以及认知功能障碍加重的病例,通过文献综述,阐明CCD的发生机制、临床特点及影响因素,为临床提供借鉴。

硫氧还蛋白1、活化T细胞趋化因子在脑梗死病人血清中的水平及与认知功能、预后的关系

目的探究硫氧还蛋白1(Trx1)、活化T细胞趋化因子(RANTES)在脑梗死病人血清中的水平及与认知功能、预后的关系。方法选取2020年3月至2022年6月在无锡市人民医院诊治的168例脑梗死病人作为观察组,及同期165例健康体检志愿者作为对照组进行研究。参照蒙特利尔认知评估量表(MoCA)评分对所有病人的认知能力进行评估,分为认知功能障碍组112例,认知功能正常组56例;根据改良Rankin量表(MRS)评分分为预后良好组90例,预后不良组78例。采用酶联免疫吸附测定(ELISA)法检测血清Trx1、RANTES水平;Spearman法分析脑梗死病人血清中Trx1、RANTES水平与MoCA评分的相关性;对影响脑梗死病人发生认知功能障碍及预后的因素进行logistic回归分析;受试者操作特征曲线(ROC曲线)分析血清Trx1、RANTES水平对脑梗死病人发生认知功能障碍的诊断价值。结果与对照组相比,观察组病人血清Trx1水平显著降低[(6.78±1.62)μg/L比(11.05±1.89)μg/L,P<0.05],RANTES水平明显升高[(35.12±4.84)ng/L比(23.51±3.28)ng/L,P<0.05];认知功能障碍组脑梗死病人血清Trx1水平明显低于认知功能正常组[(6.02±1.59)μg/L比(8.30±1.68)μg/L,P<0.05],RANTES水平显著高于认知功能正常组[(38.57±5.25)ng/L比(28.22±4.02)ng/L,P<0.05];与预后良好组对比,预后不良组脑梗死病人血清Trx1水平明显降低[(5.42±1.55)μg/L比(7.96±1.68)μg/L,P<0.05],血清RANTES水平显著升高[(38.58±5.29)ng/L比(32.12±4.45)ng/L,P<0.05];脑梗死病人血清Trx1水平与MoCA评分呈正相关(rs=0.40,P<0.05),RANTES水平与MoCA评分呈负相关(rs=−0.56,P<0.05);logistic回归分析显示,受教育程度、Trx1是影响脑梗死病人发生认知功能障碍及预后的保护因素(P<0.05),脑梗死区域、RANTES是影响脑梗死病人发生认知功能障碍及预后的危险因素(P<0.05)。ROC曲线显示,血清Trx1、RANTES、二者联合诊断脑梗死病人发生认知功能障碍的ROC曲线下面积(AUC)分别为0.82、0.94、0.97,二者联合诊断均优于其各自单独诊断(Z_(二者联合-Trx1)=4.00,P<0.001;Z_(二者联合-RANTES)=2.03,P=0.021)。结论脑梗死病人血清Trx1水平降低,RANTES水平升高,二者均与认知功能及预后有密切关系。

脑小血管病患者近期皮质下小梗死与认知功能的相关性研究

目的 探讨脑小血管病(CSVD)患者近期皮质下小梗死与认知功能的相关性。方法 回顾性连续纳入2018年2月―2022年9月就诊于北京大学第一医院神经内科经头部MRI诊断的CSVD患者,收集一般人口学资料和临床资料,使用简易精神状态量表(MMSE)、蒙特利尔认知评估量表(MoCA)评估认知功能,根据磁共振DWI分为近期皮质下小梗死(RSSI)组和非RSSI组,统计RSSI的部位和数目。比较两组患者的一般人口学资料、临床资料、认知功能,分析RSSI影像学特征与认知功能的关系。结果 共纳入CSVD患者181例,RSSI组91例,非RSSI组90例。RSSI组与非RSSI组相比,BMI高[(25.43±3.53)kg/m^(2) vs(24.27±3.33)kg/m^(2),t=2.228, P=0.027],收缩压高[(145.3±16.2)mmHg vs(139.6±20.2)mmHg,t=2.013,P=0.046],MoCA总分较低[22(18.8,26) vs 24(21,27),Z=-1.980,P=0.048],视空间与执行能力[3(2,4) vs 4(3,5),Z=-2.756,P=0.006]、语言[2(2,3) vs 2(1,2), Z=-2.020,P=0.043]、抽象[2(1,2) vs 2(1,2)分,Z=-2.052,P=0.04]得分均较低,差异均具有显著性统计学意义(P<0.05)。RSSI基底节梗死组与非RSSI组相比,MoCA总分较低[21(17,23) vs 24(21,27),Z=-2.018,P=0.044],视空间与执行[3(1.5,3.5) vs 4(3,5),Z=-2.601,P=0.009]得分较低,RSSI脑干梗死组与非RSSI组相比,视空间与执行[3(2,4) vs 4(3,5),Z=-2.325,P=0.020]、语言[2(1,2) vs 2(2,3),Z=-2.338,P=0.019]得分较低,差异具有显著性统计学意义。结论 CSVD患者中RSSI可导致认知功能障碍,与RSSI梗死部位相关,RSSI不同梗死部位导致不同的认知损害模式。预防RSSI发生,对于预防CSVD相关认知功能障碍具有重要意义。

脑梗死患者认知障碍与脑白质病变相关性分析

目的探讨脑梗死(CI)患者认知障碍与脑白质病变(WML)的相关性,基于多因素logistic回归分析认知障碍并发WML的危险因素。方法选取2020年8月至2022年10月医院收治的134例CI患者为研究对象,依据是否发生认知障碍分为发生组(56例)、未发生组(78例)。比较两组一般资料,分析认知障碍与年龄相关性脑白质改变评分(ARWMC)相关性。发生组患者依据是否发生WML病变分为非病变者36例、病变者20例,并分析WML病变者、非病变者血清学指标[视黄醇结合蛋白(RBP)、半乳糖凝集素-3(Galectin-3)、白细胞介素-33(IL-33)]水平。多因素logistic回归分析认知障碍并发WML的危险因素。评价危险因素联合预测认知障碍并发WML的预测价值。结果CI患者认知障碍与入院时ARWMC评分存在线性关系(P=0.005),且认知障碍与入院时ARWMC评分呈正相关(r=0.485,P<0.001)。病变者年龄、入院时NIHSS评分、重度颈动脉狭窄占比、多梗死灶占比高于非病变者,血清RBP、Galectin-3、IL-33水平高于非病变者(P<0.05)。高龄、入院时NIHSS评分增加、颈动脉狭窄程度加重、多梗死灶及血清RBP、Galectin-3、IL-33水平升高均为认知障碍并发WML的危险因素(P<0.05)。危险因素联合预测认知障碍并发WML的曲线下面积大于血清RBP、Galectin-3、IL-33单独预测(P<0.05)。结论CI患者认知障碍与WML呈正相关,年龄增长、入院时NIHSS评分增加、颈动脉狭窄程度增加、多梗死灶及血清RBP、Galectin-3、IL-33水平升高是影响认知障碍并发WML的危险因素,基于危险因素建立logistic回归预测模型,该模型对认知障碍并发WML具有一定预测价值。

补阳还五汤治疗脑梗死恢复期患者的临床疗效

目的:探究补阳还五汤治疗脑梗死恢复期患者的临床疗效。方法:按照治疗药物不同将84例气虚血瘀型脑梗死恢复期患者分为中药组和常规组,每组各42例。常规组采用常规药物治疗;中药组联合补阳还五汤辅助治疗。比较两组治疗前、治疗4周后的中医症候积分、神经功能、认知功能、肢体运动能力。结果:治疗4周后,两组患者中医症候积分各维度及总分、血清超敏C反应蛋白(hs-CRP)、血栓调节蛋白(TM)水平均低于治疗前,且中药组低于常规组(P<0.05);两组患者血清脱氢表雄酮(DHEA)、脑源性神经营养因子(BDNF)水平、蒙特利尔认知评估量表(MoCA)评分、Fugl-Meyer运动功能评分(FMA)均较治疗前升高(P<0.05),且中药组高于常规组(P<0.05);血清VEGF水平较治疗前降低(P<0.05),但中药组高于常规组(P<0.05)。结论:补阳还五汤可有效改善脑梗死恢复期患者临床症状,提高DHEA、BDNF水平和认知功能,促进肢体运动恢复。

外周血Lp-PLA2和FGF23水平变化与脑梗死后认知功能障碍的相关性

目的分析外周血脂蛋白相关磷脂酶A2(Lp-PLA2)、成纤维细胞生长因子23(FGF23)水平变化与脑梗死后患者认知功能障碍的相关性。方法选取2019-04—2022-12邯郸市中心医院收治的160例脑梗死患者为研究对象,根据患者是否发生认知功能障碍分为认知障碍组和非认知障碍组,对比2组基线资料及外周血Lp-PLA2、FGF23水平,并采用Logistic回归分析患者发生认知功能障碍的影响因素,采用Pearson相关性分析外周血Lp-PLA2、FGF23与简易智力状态评价量表(MMSE)评分的关系,采用ROC曲线评估外周血Lp-PLA2、FGF23对脑梗死后患者认知功能障碍的预测价值。结果160例脑梗死患者中,48例(30.00%)发生认知功能障碍。认知障碍组患者的平均年龄、高血压、糖尿病、吸烟、文化程度、MMSE评分及血清Lp-PLA2、FGF23水平等方面与非认知障碍组相比,差异有统计学意义(P<0.05)。Logistic回归分析显示,年龄、高血压、糖尿病、吸烟、文化程度低及血清Lp-PLA2、FGF23水平升高是影响脑梗死后认知功能障碍发生的独立危险因素(P<0.05)。Pearson相关性分析显示,脑梗死患者血清Lp-PLA2、FGF23水平与MMSE评分呈负相关(P<0.05)。ROC曲线显示,Lp-PLA2的曲线下面积为0.770,FGF23的曲线下面积为0.779,联合检测的曲线下面积为0.873(P<0.05),表示两者联合检测可作为评价脑梗死后认知功能障碍的有效指标。结论Lp-PLA2、FGF23在脑梗死后认知功能障碍患者血清中均呈高表达,二者联合检测有助于提高对脑梗死后认知功能障碍的预测价值。

γ-亚麻酸通过下调氧化应激反应抑制NLRP3介导的焦亡并改善脑梗塞小鼠认知障碍

目的:探究γ-亚麻酸(GLA)对脑梗塞小鼠认知障碍的影响及机制。方法:选取18只雄性小鼠,分为对照组6只、模型组6只和GLA组6只,对模型组以及GLA组以大脑中动脉闭塞术进行脑栓塞小鼠认知障碍模型制作,对照组进行假手术,即手术过程相同但不插入线栓。对照组和模型组每日以1mg/kg生理盐水灌胃,GLA组每日以1mg/kg GLA灌胃14d。以Morris水迷宫评估小鼠的认知障碍情况。处死小鼠并取小鼠大脑组织,以HE染色观察小鼠脑梗死面积,以TUNEL染色观察小鼠神经元凋亡情况,以Western Blot实验检测小鼠海马体中P22、P47、NLRP3、IL-1β、GSDMD以及Caspase-1蛋白表达水平。结果:模型组小鼠的逃逸潜伏期短于GLA组以及对照组,GLA组则短于对照组,模型组的穿越环次数最多,GLA组次之,对照组最少;模型组大脑梗死面积以及神经元凋亡数目最多,GLA组次之,对照组大脑无梗死且无神经元凋亡;模型组P22、P47、NLRP3、IL-1β、GSDMD以及Caspase-1蛋白表达高于GLA组和对照组,GLA组的蛋白表达水平则高于对照组。结论:GLA通过下调氧化应激反应抑制NLRP3介导的焦亡并改善脑梗塞导致的小鼠认知障碍。