Panax ginseng extract attenuates neuronal injury and cognitive deficits in rats with vascular dementia induced by chronic cerebral hypoperfusion

Panax ginseng is a slow-growing perennial plant.Panax ginseng extract has numerous biological activities,including antitumor,anti-inflammatory and antistress activities.Panax ginseng extract also has a cognition-enhancing effect in rats with alcohol-induced memory impairment.In this study,we partially occluded the bilateral carotid arteries in the rat to induce chronic cerebral hypoperfusion,a wellknown model of vascular dementia.The rats were then intragastrically administered 50 or 100 mg/kg Panax ginseng extract.Morris water maze and balance beam tests were used to evaluate memory deficits and motor function,respectively.Protein quantity was used to evaluate cholinergic neurons.Immunofluorescence staining was used to assess the number of glial fibrillary acidic protein-positive cells.Western blot assay was used to evaluate protein levels of vascular endothelial growth factor,basic fibroblast growth factor,Bcl-2 and Bax.Treatment with Panax ginseng extract for 8 weeks significantly improved behavioral function and increased neuronal density and VEGF and b FGF protein expression in the hippocampal CA3 area.Furthermore,Panax ginseng extract reduced the number of glial fibrillary acidic protein-immunoreactive cells,and it decreased apoptosis by upregulating Bcl-2 and downregulating Bax protein expression.The effect of Panax ginseng extract was dose-dependent and similar to that of nimodipine,a commonly used drug for the treatment of vascular dementia.These findings suggest that Panax ginseng extract is neuroprotective against vascular dementia induced by chronic cerebral hypoperfusion,and therefore might have therapeutic potential for preventing and treating the disease.

Hippocampal expression of synaptic structural proteins and phosphorylated cAMP response element-binding protein in a rat model of vascular dementia induced by chronic cerebral hypoperfusion

The present study established a rat model of vascular dementia induced by chronic cerebral hypoperfusion through permanent ligation of bilateral common carotid arteries.At 60 days after modeling,escape latency and swimming path length during hidden-platform acquisition training in Morris water maze significantly increased in the model group.In addition,the number of accurate crossings over the original platform significantly decreased,hippocampal CA1 synaptophysin and growth-associated protein 43 expression significantly decreased,cAMP response element-binding protein expression remained unchanged,and phosphorylated cAMP response element-binding protein expression significantly decreased.Results suggested that abnormal expression of hippocampal synaptic structural protein and cAMP response element-binding protein phosphorylation played a role in cognitive impairment following chronic cerebral hypoperfusion.

Expression of cyclin-dependent protein kinase 5 in the hippocampus of vascular dementia mice after cerebral ischemia and reperfusion

BACKGROUND： The p25-activated cyclin-dependent protein kinase 5 （Cdk5） may induce neuronal cell death and cause the development of dementia following cerebral ischemia and reperfusion. OBJECTIVE： To observe changes in the expression of Cdk5 and p25 in hippocampal tissue of vascular dementia mice at different time points following cerebral ischemia and reperfusion. DESIGN, TIME AND SETTING： A randomized, controlled animal experiment was performed in the clinical trial center of Hebei Provincial People＇s Hospital between September 2007 and October 2008. MATERIALS： Cdk5 rabbit anti-mouse polyclonal antibody, p35 rabbit anti-mouse polyclonal antibody, and β-actin mouse monoclonal antibody were purchased from Santa Cruz Biotechnology, Inc., USA; horseradish peroxidase-labeled goat anti-rabbit IgG and horseradish peroxidase-labeled goat anti-mice IgG were offered by Beijing Zhongshan Geldenbridye Biotechnology Co.,Ltd., China; the protein quantitative kit was produced by Applygen Gene Technology Corp., Beijing, China; cDNA reverse transcription and PCR amplification reagents were products of TianGen＆ Biotech （Beijing） Co.,Ltd., China. METHODS： One hundred and sixty male Kunming mice were randomly divided into two groups： a sham-operated group （n = 65） and a model group （n = 95）. Vascular dementia was induced with three periods of transient ischemia and reperfusion of the bilateral common carotid arteries. In the sham-operated group, the bilateral common carotid arteries were not blocked. MAIN OUTCOME MEASURES： Behavioral tests were done at four and six weeks post surgery. Pathological changes in the hippocampal CA1 region were observed with hematoxylin-eosin staining Cdk5 mRNA expression was examined by RT-PCR, and Western blots were used to evaluate Cdk5 and p25 expression. Learning and memory performance were assayed using the Morris water maze. RESULTS： Vascular dementia reduced learning and memory performance at 4 and 6 weeks post surgery. Vascular dementia also caused severe, time-dependent neuronal damage and death in the hippocampal CA1 region. Dementia induction also increased mRNA and protein expression of Cdk5 and p25 at both 4 and 6 weeks after surgery. CONCLUSION： Cdk5/p25 is involved in the development of vascular dementia in mice following cerebral ischemia and reperfusion.

EFFECT OF ELECTROACUPUNCTURE ON CEREBRAL BLOOD FLOW, VIP AND ET IN RATS WITH VASCULAR DEMENTIA

Objective: To investigate the relationship between electroacupuncture (EA)-induced improvement of regional cerebral blood flow and the alternations of vasoactive intestinal peptide (VIP) and endothelin (ET) in rats with experimental vascular dementia (VD). Methods: 40 Wistar rats were evenly randomized into sham-operation, model, medication (Nimotone) and EA groups. Vascular dementia model was established by repeated cerebral ischemia-reperfusion which was induced by occlusion and reopen of the bilateral common carotid arteries. EA (2～200 Hz, 2～3 mA) was applied to "Baihui"(GV 20), "Dazhui"(GV 14) and "Zusanli"(ST 36) for 30 min, once daily and continuously for 15 days. The regional cerebral blood flow (rCBF) in parietal lobe and hippocampus was determined with method of hydrogen clearance; a step-down avoidance test was adopted to observe the rats’ behavior change; and plasma VIP and ET contents were assayed by radioimmunoassay. Results: In comparison with sham-operation group, the correct rate of step-down avoidance test, rCBF in parietal lobe and hippocampus and plasma VIP level in VD model group lowered significantly (P<0.01) and plasma ET increased considerably (P<0.01). However, compared with model group, the correct rate of step-down avoidance test, rCBF values and plasma VIP in EA group raised obviously while plasma ET declined significantly. No significant differences were found between EA and medication groups in the 4 indexes. Conclusion: EA can raise rCBF in the parietal lobe and hippocampus, elevate plasma VIP level and reduce plasma ET in rats with VD.

The Relation between Apolipoprotein E4 Genotype and Vascular Dementia

Most studies investigating genetics of dementia have focused on Alzheimer’s disease, but little is known about the genetics of vascular dementia (VD). The aim of this study was to identify the association between Apolipoprotein E4 (Apo E4) genotype and VD in cerebrally infarcted patients. The study was conducted on 100 patients with cerebral infarction: 50 had VD (cases) and 50 didn’t have dementia (controls). Diagnosis of VD was based on Mini-Mental State Examination, Cambridge Cognitive Examination (CAMCOG), the Diagnostic and Statistical Manual of Mental Disorders 4th edition criteria for the diagnosis of VD (DSM-IV), Hachinski Ischemic Score, and computed tomography of the brain (CT brain). Apo E4 allele was assessed through DNA genotyping. The study showed that hypertension (p = 0.027, OR = 4.71), diabetes mellitus (p = 0.003, OR = 6.05) and Apo E4 allele (p = 0.017, OR = 13.39) were the independent risk factors of VD among studied participants. The study concluded that cerebrally infarcted patients with Apo E4 genotype are at high risk of developing VD.

Qinzhi Zhudan formula improves memory and alleviates neuroinflammation in vascular dementia rats partly by inhibiting the TNFR1-mediated TNF pathway

Objective: The Qinzhi Zhudan formula(QZZD) exhibits a prominent therapeutic effect in the treatment of vascular dementia(VaD). This study combined a network pharmacology approach and experimental validation to identify the underlying biological mechanism of QZZD against VaD.Methods: Male Wistar rats received bilateral common carotid artery occlusion(BCCAO) surgery, and after4 weeks of intragastric administration of QZZD, the therapeutic effect was assessed using the Morris water maze test and cerebral blood flow(CBF) assessment. Hematoxylin and eosin staining, Nissl staining, and electron microscopy were used to measure the histopathological changes in the neurons of rats. The effect of QZZD treatment on hippocampal neurotransmitters was assessed by high-performance liquid chromatography with electrochemical detection and liquid chromatography mass spectrometry.Immunofluorescence was used to observe VaD-induced microglia activation. The inflammatory cytokine levels were assessed by enzyme linked immunosorbent assay. Western blot was used to examine the TNFR1-mediated TNF pathway, which was screened out by network pharmacology analysis.Results: QZZD treatment alleviated pathological changes and neuronal damage in VaD rats and attenuated their cognitive impairment. In addition, QZZD increased CBF and the expression of acetylcholine and 5-hydroxytryptamine in the hippocampal region. Notably, QZZD inhibited microglial activation and the expression of IL-6 and TNF-a. Network pharmacology and western blot indicated that QZZD inhibited the levels of TNFR1, NF-κBp65, p-ERK, TNF-a, and IL-6, which are related to the TNFR1-mediated TNF signaling pathway.Conclusion: QZZD clearly improved learning and memory function, reduced brain pathological damage,elevated CBF and hippocampal neurotransmitter levels, and alleviated neuroinflammation of VaD rats partly by inhibiting the TNFR1-mediated TNF pathway, indicating its potential value in the clinical therapy of VaD.

Activation of glutamatergic neurons in the somatosensory cortex promotes remyelination in ischemic vascular dementia

Chronic cerebral hypoperfusion can cause progressive demyelination as well as ischemic vascular dementia,however no effective treatments are available.Here,based on magnetic resonance imaging studies of patients with white matter damage,we found that this damage is associated with disorganized cortical structure.In a mouse model,optogenetic activation of glutamatergic neurons in the somatosensory cortex significantly promoted oligodendrocyte progenitor cell(OPC)proliferation,remyelination in the corpus callosum,and recovery of cognitive ability after cerebral hypoperfusion.The therapeutic effect of such stimulation was restricted to the upper layers of the cortex,but also spanned a wide time window after ischemia.Mechanistically,enhancement of glutamatergic neuron-OPC functional synaptic connections is required to achieve the protection effect of activating cortical glutamatergic neurons.Additionally,skin stroking,an easier method to translate into clinical practice,activated the somatosensory cortex,thereby promoting OPC proliferation,remyelination and cognitive recovery following cerebral hypoperfusion.In summary,we demonstrated that activating glutamatergic neurons in the somatosensory cortex promotes the proliferation of OPCs and remyelination to recover cognitive function after chronic cerebral hypoperfusion.It should be noted that this activation may provide new approaches for treating ischemic vascular dementia via the precise regulation of glutamatergic neuron-OPC circuits.

Paeoniflorin Improves Regional Cerebral Blood Flow and Suppresses Inflammatory Factors in the Hippocampus of Rats with Vascular Dementia

Objective： To explore the delayed neuroprotection induced by paeoniflorin（PF）, the principal component of Paeoniae radix prescribed in Chinese medicine, and its underlying mechanisms in rats subjected to vascular dementia（VD）. Methods： A rat model of VD was induced by bilateral common carotid arteries occlusion（BCCAO）. Low-dose or high-dose PF（20 or 40 mg/kg once per day） was administrated for 28 days after VD. The behavioral analysis of rat was measured by water morris. Regional cerebral blood volume（r CBV）, regional cerebral blood flow（r CBF） and mean transit time（MTT） were measured in the bilateral hippocampus by perfusion-weighted imaging（PWI）. The levels of interleukin-1β（IL-1β）, interleukin-6（IL-6）, and tumor necrosis factor alpha（TNF-α） were measured by commercially available enzyme-linked immunosorbent assay kits. Protein levels were evaluated by western blot analysis. m RNA levels were evaluated by real time-polymerase chain reaction. Western blotting was used to estimate p65 translocation. Results： The behavioral analysis showed that PF could decrease the escape latency time（P〈0.05）, and increase the residence time of the original platform quadrant and the across platform frequency in water maze in VD rats（P〈0.05）. Likewise, PF remarkably promoted the r CBV（P〈0.05）, r CBF and decreased per minute MTT（P〈0.05） in hippocampus of VD rats. Furthermore, PF decreased the release of IL-1β, IL-6 and TNF-α as well as inhibited the m RNA expression of IL-1β, IL-6 and TNF-α in the hippocampus of VD rats（P〈0.05 or P〈0.01）. PF also could decrease the protein expressions of inducible nitric oxide synthase and cyclooxygenase-2 in the hippocampus of VD rats（P〈0.05 or P〈0.01）. In addition, PF significantly inhibited the nuclear factor κB（NF-κB） pathway in the hippocampus of VD rats. Conclusions： PF significantly attenuates cognitive impairment, improves hippocampus perfusion and inhibits inflammatory response in VD rats. In addition, the anti-inflammatory effects of PF might be due to inhibiting the NF-κB pathway. PF may be a potential clinical application in improving VD.

Comparative Study of the Specificities of Needling Acupoints DU20, DU26 and HT7 in Intervening Vascular Dementia in Different Areas in the Brain on the Basis of Scale Assessment and Cerebral Functional Imaging

Objective： Using methods of clinical scale assessment and cerebral functional imaging to compare the relative specificity of needling acupoints Baihui （DU20）, Shuigou （DU26） and Shenmen （HTT） in intervening vascular dementia （VD） in different areas in the brain. Methods： Fifty patients with VD were randomized into 5 groups. Needling on conventionally used acupoints of hand and foot three Yang-meridians aiming at hemiplegia was applied to the patients in Group A, and needling on DU20 to Group B, on DU26 to Group C, on HT7 to Group D and on all the three to Group E was applied additionally. Assessments of Mini Mental State Examination （MMSE）, Activities of Daily Living （ADL） and Family Attitude Questionnaire （FAQ） were made. And the positron emission computerized tomography （PET） and single photon emission computerized tomography （SPECT） examinations were conducted in 5 selected patients from each group before and after treatment. Results： Needling on conventional acupoints plus DU20 could effect the inner temporal system, thalamencephalon system and prefrontal cortical system to improve memory and executive capacity of VD patients; conventional acupoints plus DU26 could effect more to the prefrontal cortical system to obviously elevate the executive capacity; that plus HT7 would reveal an effect similar to but rather weaker than plus DU20, and effect more to memory; and that plus all the three simultaneously could effect rather roundly multiple aspects of the nervous system related to intellectual activities, to elevate the recognition and enhance the executive capacity. Conclusion： Needling on various acupoints like DU20, DU26 and HT7 have effects on different brain areas.

Arterioles in cerebral amyloid angiopathy and vascular dementia

Background Small cerebrovascular lesions are one of the most important factors in cerebral amyloid angiopathy （CAA） and vascular dementia （VaD）. We analyzed the difference of arteriolar pathology between CAA patients （CAAs） and vascular dementia patients without CAA （VaDs）. Methods Ten deceased CAAs and twelve deceased VaDs were available for this study. Five deceased patients without known cerebrovascular diseases served as controls. These patients were all autopsy cases. All transversely cut arterioles in the gray matter and white matter with an external diameter equal to or larger than 30 um and with a maximum of 300 um were examined. The internal and external diameters of arterioles were measured. Results The external diameter of gray matter arterioles in the CAAs was significantly greater than in controls. In gray matter arterioles, the diameter of the lumen in VaDs was markedly smaller than in the CAAs, whereas there was no significant difference between CAAs and controls. CAAs and VaDs may cause remarkable thickening of the arteriolar walls in either white matter or gray matter. The sclerotic index of arterioles in VaDs was significantly greater than in CAAs and controls. Conclusions Stenosis of arterioles occurred in both CAA and VaD, but the tendency was greater in VaD. Arterioles of CAA were also expanded in gray matter, which may be related to lobar hemorrhage. The loss and/or degeneration of vascular smooth muscle cells was predominant in CAA, while the over-proliferation of vascular smooth muscle cells was areater in VaD.

Specific Effects of Needling Different Acupoints of Patients with Vascular Dementia

Objective： To observe the effects of needling Baihui （GV 20）, Shuigou （GV 26） and Shenmen （HT 7） on cerebral glucose metabolism in patients with vascular dementia （VD） by cerebral functional imaging technique. Methods： Twenty-five patients with VD were divided into 5 groups （Group A, B, C, D and E） randomly. Patients in the Group A were treated by needling routine acupoints for hemiplegia （Acupoints of the three yang meridians of hand and foot）, and besides the routine acupoints, patients in the Group B were treated by needling Baihui（GV 20）, the Group C by Shuigou（GV 26）, the Group D by Shenmen（HT 7）, and the Group E by Baihui（GV 20）, Shuigou（GV 26）, and Shenmen（HT 7）. All the patients were examined by Positron Emission Tomography （PET） to detect the cerebral glucose metabolism in the bilateral frontal lobes（orbital gyri）, parietal lobes, temporal lobes（hippocampus and hippocampal gyrus）, occipital lobes, thalamus, lentiform nucleus, caudate nuclei, cingulate gyrus and cerebellum before treatments and after treatments. Results： After needling the routine acupoints for hemiplegia, glucose metabolism increased in lentiform nucleus and temporal lobe; needling Baihui（GV 20）, increased in frontal lobe, temporal lobe and lentiform nucleus; needling Shuigou（GV 26）, increased in frontal lobe, thalamus and lentiform nucleus; needling Shenmen（HT 7）, increased in parietal lobe and lentiform nucleus; and needling these three acupoints, increased in frontal lobe, temporal lobe, thalamus and lentiform nucleus. Conclusion： Needling Baihui（GV 20）, Shuigou（GV 26） and Shenmen（HT 7） affect glucose metabolism in different functional regions of the brain, and Baihui（GV 20）, Shuigou（GV26） and Shenmen（HT 7） relate to different functional regions of the brain.

不同时长运动预处理对血管性痴呆大鼠脑血流量及小胶质细胞活化相关蛋白的影响

目的:探讨不同时长运动预处理对血管性痴呆大鼠脑血流量变化及小胶质细胞活化相关蛋白的影响。方法:选用60只SPF级SD雄性大鼠,采用双侧颈总动脉永久性结扎法制备血管性痴呆大鼠模型,随机分为模型组、假手术组、运动预处理4周模型组、运动预处理4周假手术组、运动预处理2周模型组及运动预处理2周假手术组,每组10只。运动预处理4周大鼠在造模前每周行5次中等强度不负重游泳训练30min,持续4周,而运动预处理2周大鼠持续2周。利用Morris水迷宫检测大鼠空间学习记忆能力、激光散斑成像技术检测各组大鼠造模前后不同时间点脑血流变化及侧支循环开放情况、Western Blot技术检测海马TLR4及Iba1蛋白表达情况。结果:与假手术组、运动预处理2周假手术组相比,运动预处理4周假手术组、模型组、运动预处理4周模型组及运动预处理2周模型组大鼠平均逃避潜伏时延长(P<0.05)。与运动预处理4周假手术组相比,模型组、运动预处理4周模型组大鼠平均逃避潜伏时延长(P<0.05)。与模型组、运动预处理4周模型组相比,运动预处理2周模型组大鼠平均逃避潜伏时缩短(P<0.05)。重复测量方差分析简单效应提示造模前、造模后2h、造模后3d及造模后7d各组间平均脑血流量差异具有显著性意义(P<0.05)。模型组、运动预处理4周模型组及运动预处理2周模型组时间因素对平均脑血流量的简单效应具有显著性意义(P<0.01)。对各组大鼠侧支循环开放进行观察,相较于模型组,于运动预处理2周模型组观察到更少的微血管直径减少(P<0.05)。与假手术组、运动预处理4周假手术组及运动预处理2周假手术组相比,模型组Iba1、TLR4蛋白表达明显上升(P<0.01),与模型组相比,运动预处理2周模型组Iba1、TLR4蛋白表达下降(P<0.05)。结论:中等强度运动预处理2周可改善血管性痴呆大鼠学习记忆能力,运动预处理4周对学习记忆能力改善效应不明显,其机制可能与改善脑血流状态以及抑制小胶质细胞活化有关。

丁苯酞胶囊联合针刺对缺血性脑卒中后血管性痴呆患者认知功能及脑血流动力学状态的影响

目的探究丁苯酞胶囊联合针刺在缺血性脑卒中后血管性痴呆患者中的应用效果及对脑血流动力学状态及认知功能的影响。方法收集2021年3月至2023年12月于杭州市中医院就诊的缺血性脑卒中后血管性痴呆患者作为研究对象,按照不同治疗方式分为对照组(52例,行常规治疗+针刺治疗)和联合组(48例,在对照组的基础上联合丁苯酞胶囊治疗)。观察比较2组患者临床疗效、血流动力学状态[大脑中动脉血流速度(Vm)、阻力指数(RI)、脉动指数(PI)]、血清相关指标[血清降钙素基因相关肽(CGRP)、血管内皮素(ET)、缺氧诱导因子-1α(HIF-1α)]、蒙特利尔认知评估量表(MoCA)评分、生活能力量表(ADL)评分以及不良反应发生情况。结果联合组治疗总有效率为95.8%,高于对照组的82.7%(χ^(2)=4.403,P=0.036);治疗后,2组患者的MMSE评分、MoCA评分均有所升高,联合组MMSE评分、MoCA评分分别为(29.0±1.0)分、(25.9±1.0)分,均高于对照组的(27.7±1.1)分、(23.1±1.2)分(t=5.950、12.442,P<0.001);治疗后2组患者的血清相关指标均有所变化,联合组CGRP为(31±6)ng/L,高于对照组的(29±6)ng/L(t=2.266,P=0.026),联合组ET、HIF-1α分别为[(69±7)pg/ml、(254±45)pg/ml],均低于对照组的[(73±7)pg/ml、(288±52)pg/ml](t=3.413、3.479,P=0.001、0.001);治疗后联合组Vm、RI、PI分别为[(19.8±1.6)cm/s、(1.59±0.19)、(0.71±0.21)],均低于对照组的[(19.2±1.3)cm/s、RI(1.74±0.23)、PI(0.78±0.11)](t=2.121、3.539、2.111,P=0.036、0.001、0.037);治疗后,联合组ADL评分为(27±6)分,低于对照组的(31±5)分(t=4.283,P<0.001);2组患者治疗期间的不良反应发生率差异无统计学意义(χ^(2)=2.211,P=0.137)。结论丁苯酞胶囊联合针刺应用于缺血性脑卒中后血管性痴呆患者效果显著,可改善患者脑缺血性及神经损伤情况,调节血流动力参数,提高患者认知水平及日常生活能力,安全可靠,有应用价值。

脂蛋白相关磷脂酶A2联合血尿酸对急性脑梗死并发血管性痴呆的预测价值

目的探讨脂蛋白相关磷脂酶A2(Lp-PLA2)联合血尿酸对急性脑梗死并发血管性痴呆(VD)的预测价值。方法前瞻性选取哈尔滨医科大学附属第一医院收治的147例急性脑梗死住院患者,依据是否并发VD,分成VD组和无VD(nVD)组。比较2组人口学资料、临床相关资料和血清Lp-PLA2、血尿酸水平,多因素Logistic分析急性脑梗死患者并发VD的危险因素,利用受试者工作特征(ROC)曲线评价血清Lp-PLA2、血尿酸以及二者联合对急性脑梗死并发VD的预测价值。结果VD组年龄、高血压患病率、总胆固醇(TC)、Lp-PLA2[(192.38±40.16)μg/L比(148.27±35.02)μg/L]、血尿酸[(349.27±56.94)μmol/L比(293.50±48.26)μmol/L]均明显高于nVD组(P<0.05)。年龄(OR=2.017)、高血压(OR=1.381)、血清Lp-PLA2(OR=1.379)、血尿酸(OR=1.673)是急性脑梗死患者并发VD的独立危险因素(P<0.05)。血清Lp-PLA2、血尿酸预测急性脑梗死并发VD的曲线下面积(AUC)为0.785、0.734,界值为176.52μg/L、328.40μmol/L。二者联合预测的AUC为0.846(95%CI:0.737~0.955),明显高于血尿酸单独预测(P<0.05)。结论Lp-PLA2、血尿酸是急性脑梗死患者并发VD的危险因素,二者联合对急性脑梗死并发VD具有较好预测价值。

基于倾向性评分匹配法探讨急性脑梗死并发血管性痴呆的影响因素及预防建议

目的 基于倾向性评分匹配法(PSM)探讨急性脑梗死(ACI)并发血管性痴呆(VD)的影响因素,并针对性提出预防建议措施。方法 选择2019年1月—2023年1月本院收治的258例ACI患者作为研究对象,按有无发生VD分为VD组和无VD组两组,匹配前,VD组54例无VD组204例;匹配后,VD组52例无VD组52例。比较匹配前后两组一般资料;基于PSM匹配两组资料,采用Logistic回归模型分析匹配后ACI并发VD的影响因素。结果 258例患者中54例发生VD,VD发生率为20.93%;匹配前,VD组患者受教育年限短于无VD组,差异有统计学意义(P<0.05);VD组患者高血压、高脂血症、糖尿病、脑梗死病史、额叶脑梗死、脑白质疏松构成比及入院时NIHSS评分高于无VD组,差异有统计学意义(P<0.05);VD组患者脑梗死面积大于无VD组,差异有统计学意义(P<0.05);VD组患者ACI发病至入院时间长于VD组,差异有统计学意义(P<0.05);VD组患者出院后康复治疗构成比低于无VD组,差异有统计学意义(P<0.05);匹配后,VD组患者受教育年限短于无VD组,差异有统计学意义(P<0.05);VD组患者高血压、额叶脑梗死构成比及入院时NIHSS评分高于无VD组,差异有统计学意义(P<0.05);VD组患者脑梗死面积大于无VD组,差异有统计学意义(P<0.05);VD组患者ACI发病至入院时间长于无VD组,差异有统计学意义(P<0.05);VD组患者出院后康复治疗构成比低于无VD组,差异有统计学意义(P<0.05);Logistic回归模型分析显示受教育年限、高血压、额叶脑梗死、脑梗死面积、出院后康复治疗是ACI并发VD的影响因素(P<0.05)。结论 基于PSM法发现受教育年限、高血压、额叶脑梗死、脑梗死面积、出院后康复治疗是ACI并发VD的影响因素。

高压氧联合银杏叶提取物治疗老年血管性痴呆疗效观察

目的探讨高压氧联合银杏叶提取物治疗老年血管性痴呆的临床疗效。方法选择2019年1月至2022年12月在郑州市第九人民医院就诊的132例老年血管性痴呆患者为研究对象,采用随机数字表法将患者分为观察组和对照组,每组66例。2组患者均给予常规治疗,在此基础上,对照组患者给予高压氧治疗,每日1次;观察组患者给予高压氧联合银杏叶提取物治疗,每日1次;2组患者均连续治疗1个月。分别于治疗前后采用蒙特利尔认知评估量表(MoCA)和Barthel指数评估2组患者的认知功能和日常生活活动能力,并依据MoCA评分和Barthel指数评估2组患者治疗后的临床疗效。分别于治疗前后采用经颅多普勒超声仪检测2组患者大脑前动脉、大脑后动脉、大脑中动脉及椎动脉平均血流速度等脑血流动力学指标。结果治疗前2组患者MoCA评分及Barthel指数比较差异无统计学意义(P>0.05)。治疗后,2组患者MoCA评分及Barthel指数均高于治疗前(P<0.05),且观察组患者的MoCA评分及Barthel指数显著高于对照组(P<0.05)。治疗后,对照组和观察组患者总有效率分别为84.85%(56/66)和95.45%(63/66),观察组患者总有效率显著高于对照组(χ^(2)=4.181,P<0.05)。治疗前2组患者大脑前动脉、大脑后动脉、大脑中动脉及椎动脉平均血流速度比较差异无统计学意义(P>0.05)。治疗后,2组患者大脑前动脉、大脑后动脉、大脑中动脉及椎动脉平均血流速度大于治疗前(P<0.05),且观察组患者大脑前动脉、大脑后动脉、大脑中动脉及椎动脉平均血流速度大于对照组(P<0.05)。治疗期间对照组和观察组患者总不良反应发生率分别为16.67%(11/66)、18.18%(12/66),2组患者总不良反应发生率比较差异无统计学意义(χ^(2)=0.218,P>0.05)。结论高压氧联合银杏叶提取物可更显著地改善老年血管性痴呆患者脑血流状态和认知功能障碍,提高患者日常生活活动能力,总体疗效好,且安全性高。

灯盏生脉胶囊联合针刺对脑梗死后血管性痴呆患者的临床疗效

目的考察灯盏生脉胶囊联合针刺对脑梗死后血管性痴呆患者的临床疗效。方法300例患者随机分为对照组和观察组,每组150例,2组采用常规治疗,同时对照组给予针刺,观察组在对照组基础上加用灯盏生脉胶囊,疗程3个月。检测临床疗效、中医证候评分、MoCA评分、ADAS-cog评分、TNF-α、GSH-Px、AOPP、血流速度(大脑中动脉、大脑后动脉、大脑前动脉)、Hcy、BDNF、NPAS4变化。结果观察组总有效率高于对照组(P<0.05)。治疗后,2组中医证候评分、ADAS-cog评分、TNF-α、AOPP、Hcy、NPAS4降低(P<0.05),MoCA评分、GSH-Px、BDNF升高(P<0.05),动脉血流速度增加(P<0.05),以观察组更明显(P<0.05)。结论灯盏生脉胶囊联合针刺可减少脑梗死后血管性痴呆患者氧化应激损伤及炎症反应,改善脑血流,缓解神经元损伤,促进认知功能和病情恢复。

三七通舒胶囊联合奥拉西坦治疗脑梗死后血管性痴呆的临床效果及对血液流变学指标的影响

目的:探讨脑梗死(CI)后血管性痴呆(VD)采用三七通舒胶囊联合奥拉西坦治疗的临床效果及对血液流变学指标的影响。方法:选取2021年1月—2023年1月辽宁省金秋医院收治的共计102例CI后VD患者,以随机数字表法分成研究组(n=51)与对照组(n=51),对照组给予奥拉西坦治疗,研究组给予三七通舒胶囊联合奥拉西坦治疗,均治疗2个月。比较两组临床疗效、痴呆程度、血液流变学、认知功能及日常生活能力。结果:研究组治疗总有效率(92.16%)较对照组(76.47%)高,差异有统计学意义(P<0.05);治疗后两组临床痴呆评定量表(CDR)评分均降低(P<0.05),研究组较对照组低,差异有统计学意义(P<0.05);治疗后两组全血低切黏度、全血高切黏度、血浆黏度均降低(P<0.05),研究组均较对照组低,差异均有统计学意义(P<0.05);治疗后两组简易智能精神状态量表(MMSE)、蒙特利尔认知评估量表(MoCA)、Barthel指数评分均升高(P<0.05),研究组均较对照组高,差异均有统计学意义(P<0.05)。结论:三七通舒胶囊联合奥拉西坦用于治疗CI后VD,能够提高临床效果,减轻痴呆程度,改善血液流变学,促进认知功能、日常生活能力提高。

急性脑梗死合并血管性痴呆患者认知功能与血清NRG-1、Lp-PLA2水平的相关性分析

目的探讨急性脑梗死合并血管性痴呆患者认知功能与血清神经调节蛋白1(NRG-1)、脂蛋白磷脂酶a2(Lp-PLA2)水平的相关性。方法在连云港市第一人民医院2019年1月—2022年1月收治的急性脑梗死合并血管性痴呆患者中选取102例,采用蒙特利尔认知评估量表(MoCA)评估认知功能,并根据评分情况分为轻中度组、重度组,对比两组一般资料[年龄、性别、体重指数(BMI)、血管性痴呆家族史、吸烟史、饮酒史、基础合并症]、血清指标(NRG-1、Lp-PLA2),绘制受试者工作特征(ROC)曲线分析NRG-1、Lp-PLA2对急性脑梗死合并血管性痴呆患者认知功能的评估价值,采用多因素Logistic回归分析明确重度认知功能障碍的危险因素。结果两组年龄、性别、BMI、血管性痴呆家族史、吸烟史、饮酒史等一般资料比较无统计学意义(P>0.05),轻中度组NRG-1水平高于重度组、Lp-PLA2水平低于重度组(P<0.05);经ROC分析证实NRG-1、Lp-PLA2能够用于评估急性脑梗死合并血管性痴呆患者认知功能,曲线下面积分别为0.952、0.655,P<0.05;多因素Logistic回归分析证实NRG-1≤196.36 pg/mL、Lp-PLA2≥147.33 ng/mL为急性脑梗死合并血管性痴呆患者重度认知功能障碍的危险因素(P<0.05)。结论对于急性脑梗死合并血管性痴呆患者可通过检测血清NRG-1、Lp-PLA2水平评估认知功能,NRG-1水平降低、Lp-PLA2水平升高可用做评估患者认知功能重度障碍的指标。

中药香薰法治疗脑萎缩、小脑萎缩、血管性痴呆、老年痴呆及帕金森病验案

随着社会老龄化问题加剧,神经退行性疾病发病率持续上升,已经成为全球性公共卫生难题。目前尚无明确的预防或治疗方法来减缓此类疾病的进展,本文对中药香薰法治愈1例发病早期患者的相关过程进行分析。由于人类脑神经元是长寿细胞,不会自然衰老死亡,因此提出脑萎缩、小脑萎缩、血管性痴呆、老年痴呆、帕金森病是因脑动脉循环障碍等造成脑血流灌注不足,导致迟发性脑神经元凋亡而引发的以痴呆为主的系列症状。中药香薰法可增加脑血流灌注量,改善大脑缺血状态,激活处于睡眠状态、凋亡的脑神经元,治疗早期神经退行性疾病可促使患者基本恢复正常,治疗中晚期患者也可以阻止病情发展,保持脑神经元的数量,进而延长其寿命。