急性脑梗死患者血清骨桥蛋白水平的改变及其对预后的影响

目的探究急性脑梗死患者血清骨桥蛋白水平的变化及其对预后的影响。方法详细收集112例急性脑梗死患者及53例健康对照组的临床资料并通过ELISA法测定患者1 d、7 d、12 d血清骨桥蛋白水平,计算脑梗死患者梗死面积,并进行NIHSS评分、TOAST及OCSP分型,采用Pearson相关分析法分析7 d血清骨桥蛋白水平与各危险因素的相关性,根据mRS评分将脑梗死患者分为预后良好组(2分)及预后不良组(2分),比较两亚组血清骨桥蛋白水平,进行Logistic回归分析,探讨其在急性脑梗死预后中的作用。结果急性脑梗死患者7 d血清骨桥蛋白水平较对照组显著升高[(8.05±5.47)ng/ml vs(5.05±2.37)ng/ml,P0.01]。其水平与入院时梗死面积(r=0.254,P=0.007),NIHSS评分(r=0.233,P=0.013)均呈正相关。在Logistic回归分析中,我们发现骨桥蛋白水平6.565 ng/ml是不良预后的独立危险因素(OR=3.207,95%CI 1.212~8.485,P=0.019)。结论骨桥蛋白参与缺血性脑卒中的病理生理过程,可以作为评价急性脑梗死预后的一个重要的生物学指标。     

血清血管生成素1水平与急性脑梗死发病、病情严重程度及90 d预后的关系

目的探讨血清血管生成素1(Ang-1)水平与急性脑梗死发病、病情严重程度及90 d预后的关系。方法对132例急性脑梗死患者(病例组)及108名健康体检者(对照组)进行血清Ang-1水平检测,同时采集相关的临床资料。病例组入院时进行NIHSS评分,将NIHSS评分5分者定义为病情轻度组,5~15分为病情中度组,≥16分为病情重度组。病例组90 d后随访行mRS评分,将mRS评分≤2分者定义为预后良好组,2分者定义为预后不良组。结果病例组吸烟史、高血压病、糖尿病、心房纤颤的比例明显高于对照组,血清Ang-1水平明显低于对照组(均P0.05)。Logistic回归分析显示,糖尿病及血清Ang-1水平均与急性脑梗死的发病密切相关(均P0.01)。病情轻度组患者血清Ang-1水平[(1.12±0.35)ng/ml]与病情中度组[(0.96±0.39)ng/ml]、病情重度组[(0.76±0.49)ng/ml]比较,差异有统计学意义(P=0.003)。进一步分析显示,急性脑梗死患者病情严重程度与血清Ang-1水平呈负相关(r=-0.267,P=0.002)。预后不良组患者的入院时NIHSS评分、高血压病、糖尿病、心房纤颤的比例均明显高于预后良好组,而血清Ang-1水平明显低于预后良好组显著降低(均P0.05)。Logistic回归分析显示,入院时NIHSS评分及血清Ang-1水平均与急性脑梗死患者90 d预后密切相关(均P0.01)。结论急性脑梗死患者的血清Ang-1水平较低,且血清Ang-1水平与急性脑梗死的发病、病情严重程度及90 d预后均密切相关。     

血清血管生成素1水平与急性脑梗死严重程度的相关性

目的 探讨患者血清血管生成素1(Ang-1)水平与急性脑梗死的严重程度的相关性,为临床早期病情评估提供依据.方法 收集西安市第九医院诊断为急性脑梗死的患者为病例组,同时收集本院同期体检中心的健康体检者为对照组.收集所有研究对象的一般临床资料,并测定血清Ang-1水平.病例组分别根据美国国立卫生研究院脑卒中量表(NIHSS)评分及MRI最大梗死直径分组.比较病例组与对照组一般临床资料的差异.采用Logistic回归分析病例组的发病危险因素.通过ROC曲线评估血清Ang-1水平的诊断价值.采用Spearman相关分析脑梗死严重程度与Ang-1的相关性.结果 病例组患者的吸烟史、高血压病史、糖尿病史及心房纤颤病史的比例高于对照组,而血清Ang-1水平低于对照组,差异有统计学意义(P<0.05).Logistic回归分析显示,糖尿病史及血清Ang-1水平是急性脑梗死的危险因素(P<0.05).ROC曲线分析显示血清Ang-1水平在诊断急性脑梗死患者时的曲线下面积为0.791(95%CI=0.751~0.830).NIHSS评分为轻度、中度及重度组患者的血清Ang-1水平分别为(1.65±0.22)ng/ml,(1.45±0.24)ng/ml和(1.26±0.27)ng/ml,差异有统计学意义(F=47.940,P<0.01).MRI显示大梗死、中梗死及小梗死组患者的血清Ang-1水平分别为(1.38±0.23)ng/ml,(1.49±0.30)ng/ml和(1.71±0.23)ng/ml,差异有统计学意义(F=40.911,P<0.01).Spearman相关性分析显示急性脑梗死患者入院时NIHSS评分及MRI梗死最大直径与血清Ang-1水平均呈负相关(r=-0.498,-0.459;P<0.01).结论 脑梗死患者的血清Ang-1水平下降,并与脑梗死的严重程度密切相关.     

急性脑梗死患者血浆CXCL12水平的改变及其对预后的影响

目的探讨急性脑梗死患者血浆CXCL12水平的改变及其对预后的影响。方法采用ELISA法检测185例急性脑梗死患者(脑梗死组)及123例正常体检者(对照组)的血浆CXCL12水平。对脑梗死患者进行NIHSS评分及mRS评分,采用Pearson相关性分析法分析脑梗死组患者血浆CXCL12水平与NIHSS评分的相关性。根据mRS评分,将脑梗死组患者分为预后良好亚组(mRS评分0~2分)和预后不良亚组(mRS评分3~6分),比较两亚组患者的血浆CXCL12水平,并进行Logistic回归分析。结果脑梗死组患者血浆CXCL12水平[(3.75±1.40)μg/ml]明显高于对照组[(0.96±0.67)μg/ml](P0.01)。Pearson相关性分析显示,脑梗死组患者血浆CXCL12水平与入院时NIHSS评分呈负相关(r=-0.857,P0.01)。预后良好亚组患者血浆CXCL12水平[(4.56±1.24)μg/ml]明显高于预后不良组[(2.75±0.84)μg/ml](P0.01)。Logistic回归分析结果显示,血浆CXCL12水平升高是预后不良的独立保护因素(OR=0.416,95%CI:0.225~0.768,P=0.005)。结论急性脑梗死患者的血浆CXCL12水平升高,是其预后不良的独立保护因素。血浆CXCL12水平可作为评价急性脑梗死预后的一个重要的生物学指标。     

血浆和肽素水平对急性脑梗死患者预后的评估价值

目的 探讨血浆和肽素水平对急性脑梗死患者预后的评估价值.方法 对60例急性脑梗死患者(急性脑梗死组)和60例健康体检者(正常对照组)进行血浆和肽素水平检测;并对急性脑梗死患者进行血压、血糖、血清超敏C反应蛋白(hs-CRP)水平检测,应用美国国立卫生研究院卒中量表(NIHSS)进行评分,应用MRI测量脑梗死体积,3个月后采用改良的Rankin量表(mRS)评分评价预后;分析血浆和肽素水平对急性脑梗死患者预后的影响.结果 急性脑梗死组血浆和肽素水平[( 3.73±0.49) ng/ml]明显高于正常对照组[ (2.85±0.24) ng/ml](P＜0.01);脑梗死预后不良亚组(42例)[(3.84±0.44) ng/ml]明显高于预后良好亚组(18例)[ (3.47±0.53) ng/ml] (P＜0.05);两亚组间年龄、血糖、血清hs-CPR水平、NIHSS评分、脑梗死体积的差异有统计学意义(P ＜0.05 ～0.01);单因素Logistic回归分析显示,血浆和肽素水平、年龄、NIHSS评分是影响急性脑梗死患者预后的因素(P ＜0.05 ～0.01).ROC分析显示,影响急性脑梗死患者预后的因素中,血浆和肽素水平与年龄、hs-CRP水平、脑梗死体积、NIHSS评分间差异无统计学意义.结论血浆和肽素水平升高是预测急性脑梗死患者预后不良的因素之一.     

急性脑梗死患者血清白介素-18和组织因子水平变化及其与凝血功能的关系

目的 探讨急性脑梗死(ACI)患者血清白介素(IL)-18和组织因子(TF)水平的变化及其与凝血功能关系.方法 79例ACI患者(ACI组)于入院次日、25名健康体检者(正常对照组)于体检当日早晨,分别检测血清IL-18、TF水平和凝血功能.结果 ACI组患者的血清IL-18、TF水平[(282.22±127.45)pg/ml,(2.10±1.23)ns/ml]明显高于正常对照组[(131.13±37.17)pg/ml,0.67±0.34)ng/ml](P<0.01～0.001):ACI组患者凝血功能指标中的部分凝血活酶时间及纤维蛋白原(Fib)水平显著高于正常对照组(均P<0.05);ACI组患者血清TF水平与凝血酶原时间及Fib水平呈正相关(r=0.376,r=0.473,P<0.05～0.01).结论 血清IL-18与TF水平异常增高是参与动脉粥样硬化相关性血栓形成的重要原因之一,抗凝及降纤治疗通过抑制TF水平逆转该病理过程.     

脑出血患者血清骨桥蛋白水平的变化及其对预后的影响

目的探究脑出血患者血清骨桥蛋白水平的变化及其对预后的影响。方法收集61例脑出血患者(脑出血组)及54名健康对照者(对照组)的临床资料,采用ELISA法测定血清骨桥蛋白水平。脑出血组患者于入院后24 h内进行脑出血评分,根据CT计算脑出血体积,于发病3个月后行mRS评分。对结果进行分析比较。结果脑出血组患者血清骨桥蛋白水平[(7.69±5.10)ng/ml]明显高于对照组[(5.58±3.12)ng/ml](P=0.008)。脑出血组中预后良好亚组(mRS评分4分)36例(59.02%),预后不良亚组(mRS评分≥4分)25例(40.98%)。预后不良亚组WBC、脑出血体积、脑出血破入脑室比例、脑出血评分及血清骨桥蛋白浓度均明显高于预后良好亚组(均P0.05)。ROC曲线分析示,血清骨桥蛋白水平的截断点为7.57 ng/ml时,曲线下面积为0.634,灵敏度为0.720,特异度为0.611。多因素Logistic回归分析显示,血清骨桥蛋白水平7.57 ng/ml(OR=4.045,95%CI:1.143~14.320,P=0.030)、脑出血破入脑室(OR=5.236,95%CI:1.009~27.172,P=0.049)是脑出血预后不良的独立危险因素。结论急性脑出血患者血清骨桥蛋白水平升高,是其预后不良的独立危险因素,可以作为评价脑出血预后的一个重要的生物学指标。     

血清miR-17-5p与Hcy水平联合预测急性缺血性脑卒中患者预后的价值

目的探讨血清miR-17-5p及同型半胱氨酸(Hcy)水平联合预测急性缺血性脑卒中(AIS)患者预后的价值。方法选取2016年1月至2019年3月儋州市人民医院收治的158例AIS,根据改良Rankin量表(mRS)评分将患者分为预后良好组(n=98,mRS评分≤2分)和预后不良组(n=60,mRS评分2分),采用美国国立卫生研究院卒中量表(NIHSS)评分将患者分为轻度组(n=47,NIHSS评分5分)、中度组(n=73,5分≤NIHSS评分≤20分)、重度组(n=38,NIHSS评分20分)。检测各组血清miR-17-5p及Hcy水平,应用ROC曲线分析miR-17-5p联合Hcy预测AIS患者预后不良的价值。采用Pearson相关分析方法分析AIS患者血清miR-17-5p及Hcy水平与NIHSS及mRS评分的相关性。结果 AIS组血清miR-17-5p[(2.38±0.74)比(0.24±0.08)]及Hcy[(18.60±5.30)μmol/L比(5.70±1.15)μmol/L]水平明显高于对照组(均P0.01)。预后不良组血清miR-17-5p[(3.24±1.08)比(1.56±0.63)]及Hcy[(23.40±6.10)μmol/L比(14.25±3.58)μmol/L]水平明显高于预后良好组(均P0.01)。重度组血清miR-17-5p[分别为:(3.60±1.15)比(2.52±0.90),(3.60±1.15)比(1.20±0.47)]及Hcy[(28.20±6.74)μmol/L比(18.36±4.82)μmol/L,(28.20±6.74)μmol/L比(11.35±3.20)μmol/L]水平均明显高于中度组和轻度组(P0.01),且中度组血清miR-17-5p[(2.52±0.90)比(1.20±0.47)]及Hcy[(18.36±4.82)μmol/L比(11.35±3.20)μmol/L]水平均明显高于轻度组(P0.01)。ROC曲线分析显示,血清miR-17-5p及Hcy水平预测AIS患者预后不良的最佳截值分别为2.06、17.62μmol/L,两项联合预测AIS患者预后不良的曲线下面积[0.918(95%CI:0.860～0.975)]较高,其敏感度和特异度分别为92.0%和85.3%。相关分析结果显示,预后不良组血清miR-17-5p及Hcy水平与NIHSS(分别r=0.772、0.853,P0.01)及mRS评分(分别r=0.740、0.807,P0.01)均呈正相关。结论血清miR-17-5p及Hcy水平升高与AIS患者神经功能缺损的严重程度及预后不良相关,且miR-17-5p联合Hcy对AIS患者预后预测具有较高的价值。     

血清铁蛋白水平对急性缺血性脑卒中患者出血转化的预测价值

目的探讨血清铁蛋白水平对急性缺血性脑卒中患者发生出血转化(HT)的预测价值。方法 189例急性缺血性脑卒中患者根据CT复查结果分为HT组和非HT(non-HT)组,同时将HT组分为出血性梗死(HI)亚组和脑实质血肿(PH)亚组。采用ELISA法检测患者发病48 h内血清铁蛋白水平,比较各组血清铁蛋白水平,评估其对HT的预测意义。结果 CT结果显示,189例急性缺血性脑卒中患者中发生HT者87例(46%),其中HI 66例、PH 21例。HT组血清铁蛋白水平[(175.49±109.09)ng/m L]明显高于non-HT组[(117.25±78.42)ng/m L](P0.01)。PH亚组血清铁蛋白水平[(245.18±103.63)ng/m L]明显高于HI亚组[(153.31±101.84)ng/m L](P0.01)。多因素Logistic回归分析显示,血清铁蛋白水平升高是急性缺血性脑卒中患者发生HT的独立危险因素(OR=1.004,95%CI:1.000~1.008,P=0.029),同时也是发生PH的独立危险因素(OR=1.006,95%CI:1.001~1.011,P=0.021)。血清铁蛋白水平预测急性缺血性脑卒中患者发生HT和PH的ROC曲线下面积分别为0.687(95%CI:0.611~0.763,P0.001)、0.782(95%CI:0.652~0.913,P0.001),预测值分别为131.5 ng/ml、182.0 ng/ml。结论血清铁蛋白水平升高是急性缺血性脑卒中患者发生HT、PH的独立危险因素。血清铁蛋白水平对急性缺血性脑卒中患者发生HT具有预测价值。     

P-选择素、血管内皮生长因子在皮质下动脉硬化性脑病中的表达及意义

目的探讨皮质下动脉硬化性脑病(SAE)患者血P-选择素、血管内皮生长因子(VEGF)水平及其与血糖、血脂和C反应蛋白(CRP)的相关性。方法测定54例SAE患者(SAE组)、57名健康老年人(健康对照组)血浆P-选择素、血清VEGF、血糖、血脂、CRP水平,并进行比较和相关分析。结果SAE组P-选择素[(17.61±5.63)ng/ml]、VEGF[(126.33±47.51)pg/ml]水平明显高于健康对照组[(14.72±3.89)ng/ml,(102.59±40.16)pg/ml](均P<0.01);P-选择素水平随痴呆程度加重而升高,痴呆中、重度组VEGF水平[(152.46±53.75)pg/ml、(150.52±55.94)pg/ml]明显高于轻度组[(126.79±44.83)pg/ml](P<0.01,P<0.05);中、重度组间差异无统计学意义。SAE组P-选择素与血糖、三酰甘油(TG)、CRP呈正相关(r=0.282、0.293、0.287,均P<0.05);VEGF与总胆固醇(TC)、CRP呈正相关(r=0.291、0.336,均P<0.05);P-选择素与VEGF呈正相关(r=0.295,P<0.05)。结论P-选择素、VEGF参与了SAE的血栓形成和组织修复过程;检测P-选择素、VEGF水平,指导抗血小板药物的应用,对预防SAE可能有重要意义。     

脑梗死静脉溶栓治疗后出血性转化临床分析

目的探讨急性脑梗死患者溶栓治疗后出血性转化(hemorrhagic transformation,HT)的危险因素以及继发HT患者的溶栓后并发症。方法回顾性分析62例经静脉溶栓治疗的急性脑梗死患者的临床资料,结合文献选择溶栓后继发HT的危险因素,包括年龄、性别、高血压、糖尿病、心功能不全史、脑卒中史、有无早期CT缺血改变、是否大面积脑梗死、是否心源性脑栓塞、发病至溶栓时间、溶栓药物、溶栓前NIHSS评分、溶栓前血糖水平、溶栓后3d内最低纤维蛋白原水平、血小板计数、肌酐水平等进行分析,对单因素分析法发现有统计学差异的危险因素进一步行Logistic回归分析。结果单因素分析发现,与无HT组相比,继发HT组年龄较大(P<0.01),溶栓前血糖水平(P<0.05)、溶栓后6h和12h的收缩压和舒张压较高(均P<0.05),大面积脑梗死发病至溶栓时间>3h、有早期CT缺血改变的患者比例高(均P<0.05)。Logistic多因素回归分析发现高龄(OR:1.129,P<0.05)、溶栓时间>3h(OR:2.592,P<0.05)、早期CT有缺血改变(OR:1.728,P<0.05)是继发HT的危险因素。继发HT组出现颅外出血并发症(52.2%vs 20.5%,χ2=6.637,P<0.05)、重度脑水肿(30.4%vs 5.1%,χ2=5.567,P<0.05)和脑疝形成(26.1%vs 2.6%,P<0.05)的比例更高。结论急性脑梗死患者静脉溶栓后HT的发生率高,高龄、发病至溶栓时间>3h和早期CT缺血改变是HT的危险因素。     

胰岛素抵抗与正常血压脑出血及脑梗塞关系的探讨

为研究胰岛素抵抗与脑出血、脑梗塞的关系,测定了正常血压脑出血41例、正常血压脑梗塞51例及对照组39例的血清胰岛素与血糖比值I/G,结果显示:三组I/G分别为6.3098±8.3268,5.1867±3.0069和2.4091±1.1374(means±SD)。正常血压脑出血组与对照组比较P<0.01。正常血压性脑梗塞组与对照组比较P<0.05。认为胰岛素抵抗是脑出血、脑梗塞的危险因素。     

Regional cerebral blood flow after occlusion of the middle cerebral artery

Occlusions of the middle cerebral artery (MCA) are mostly of embolic origin (appr. 80%) and give rise to about one third of all ischemic strokes, most of these being major strokes. MCA occlusions lasting for less than 1/2 h are tolerated without occurrence of permanent tissue damage. Occlusions lasting between 1/2 h to 4-8 h lead to permanent tissue damage and neurological deficits that are proportional to the duration of occlusion. Maximal tissue damage is obtained after 4-8 h occlusion. A cerebral blood flow of 8-23 ml/100 gr/min is sufficient for cellular viability but insufficient for normal tissue function ("ischemic penumbra"). Cellular function is completely abolished in the interval 8-16 ml/100 gr/min and flow at that level is tolerated only for 1-3 h before neuronal death ensues. In the interval 18-23 ml/100 gr/min there is some functional activity although it is reduced. Experimental and clinical evidence suggests that flow in this interval may be tolerated for several days, months or even longer ("chronic ischemic penumbra"). After MCA occlusion the blood flow falls below 8 ml/100 gr/min in most cases and permanent MCA occlusion always leads to relatively large areas of frank infarction. The ischemic infarcts may be surrounded by collaterally perfused areas where the blood flow is pressure-dependent (impaired autoregulation) and quite commonly insufficient for normal neuronal function (below 23 ml/100 gr/min). Such collaterally perfused areas may include a "chronic ischemic penumbra". Emboli causing MCA occlusions commonly disintegrate and/or migrate more peripherally within the first few weeks post stroke. This leads to reperfusion and changes of ischemic infarcts into hyperemic infarcts where flow is severely increased. The vascular reactivity is completely abolished in hyperemic infarcts and the hyperemic state lasts for about two weeks. Probably, anemic infarcts are equivalent to ischemic infarcts while the hemorrhagic variety is equivalent to hyperemic infarcts. The "partial infarct" with selective neuronal necrosis occurs in experimental animals after MCA occlusions of less than four h but not after permanent MCA occlusion. The significance of partial infarction in human stroke is not clarified. The extent of irreversible tissue damage can be reduced only if therapy sets in within 4-8 h after the occlusion. If a "chronic penumbra" exists the extension of reversible tissue damage can be reduced if therapy aimed at increasing the blood flow in the penumbra sets in within weeks or even months after the stroke.(ABSTRACT TRUNCATED AT 400 WORDS)     

神经功能缺损评分的比较研究--193例资料分析

目的比较3种神经功能缺损评分在评价脑血管病临床轻重程度、预后转归的相关性.方法应用<中国卒中患者神经功能缺损评分标准>(CSS)、<美国国立卫生研究所脑卒中评分>(NIHSS)与<加拿大神经功能评分>(CNS)对193例急性脑血管病临床轻重程度、预后转归进行评价.结果3种神经功能评分均能对不同程度和类型脑血管病人作出临床评定,但CNS评分数据变异小,能较客观评价不同部位出血和特殊部位脑梗死的临床状况;CSS与CNS和NIHSS评价病情轻重和转归有同等价值,相关性较好.结论CSS能较好反映脑血管病人的病情轻重程度和21d的疾病转归情况,与NIHSS、CNS有很好的相关性.     

Distribution of cerebral microembolism in the anterior and middle cerebral arteries

BACKGROUND AND PURPOSE: Cerebral infarcts occur more frequently along the middle (MCA) than the anterior cerebral artery (ACA) territory. The reason(s) for this difference remains speculative. The objective of this study was to investigate the distribution of cerebral microemboli as detected by transcranial Doppler ultrasound (TCD) along the MCA and ACA territories. METHODS: Records of consecutive patients examined for the presence of cerebral microembolism during a 32-month period at the Neurovascular Laboratory were reviewed. Of the original 375 TCD studies in 268 patients, 28 studies in 24 patients demonstrated microembolic signals (MES) and monitored the MCA and ACA on the same side. TCD studies were performed on TC-2000 or TC-2020 instruments. MES positive studies were saved and off-line reviewed. MES satisfied previously established criteria. RESULTS: MES were more frequent in the MCA than the ACA in 85.7% (24/28) of studies (P < 0.01). Of the total number of MES (n = 979), 29.6% (n = 290) were detected in the ACA and 70.4% (n=689) in the MCA (P<0.01). The mean (+/- SD) intensity of MCA MES of 12.2 (+/- 2.4) dB was significantly lower than that of ACA MES of 14.8 (+/-3.2) dB (P=0.05). The mean (+/-SD) duration of MCA MES of 38.1 (+/- 45.3) ms was longer than that of ACA MES of 30.7 (+/-34.0) ms (P=0.05). CONCLUSIONS: Cerebral microembolism occurs more frequently in the MCA than the ACA, which may explain the uneven distribution of cerebral infarcts along these arterial territories. Furthermore, there are significant differences in the characteristics of ACA and MCA MES.     

Attitudes in the management of acute ischaemic cere-brovascular accident and cerebral haemorrhage in Latin America: a multinational study

ABSTRACT— Eleven neurologists (the Collaborative Group) from 7 Latin American countries interviewed 73 of their peers (respondents) with a questionnaire containing points on history-taking, investigations performed, and treatment. The obvious methodological pitfalls of this method are discussed. It was felt, nevertheless, that with judicious interpretation of the answers a fair reflection of reality can be obtained. Items in the history which are less frequently enquired for were alcohol intake just before a stroke, known abnormalities in the blood picture, and intermittent claudication. Amongst less frequently performed investigations were Doppler study of carotids, angiography, lumbar puncture, echocardiography ordered without the indication of a cardiologist, and EEG. Regarding treatment, steroids were preferred by a large majority in the treatment of cerebral oedema. In other items two thirds or more of respondents reached agreement except when dealing with high blood pressure on admission, the use of aspirin in acute ischaemic non-cardiogenic stroke and the use of anticoagulants in stroke considered to be progressing. No differences by country or years of experience were found. The management of affluent and poorer patients was more even than might be expected, most telling differences being CT scanning and anticoagulation.     

Point/counterpoint: We should not take the direction of blood pressure change into consideration for dynamic cerebral autoregulation quantification

Over the past years, a wide range of studies have provided evidence of asymmetry in the response of static and dynamic cerebral autoregulation (CA) during increasing and decreasing pressure challenges. The main message is that CA is stronger during transient increases of arterial blood pressure rather than decreases. Here we do not argue against the presence of CA asymmetry but we seek to raise questions regarding the measurement of the effect and whether this effect needs to be taken into account, especially in clinical settings.     

Cerebral metabolic and circulatory changes in the rat during sustained seizures induced by DL-homocysteine

Sustained, generalized seizure activity was induced in anaesthetized (70% N2O), paralyzed and artifically ventilated rats by i.p. DL-homocysteine thiolactone in a dose of 11 mmol/kg. Epileptic discharges in the EEG were accompanied by marked perturbation of tissue metabolites. There was a fall in phosphocreatine concentration to 40% of control but only moderate changes in adenine nucleotides, a marked rise in lactate concentration, and a pronounced increase in the lactate/pyruvate ratio. Excessive amounts of dihydroxyacetone phosphate (and glyceraldehyde phosphate) accumulated, indicating that depletion of NAD+ occurred. There was marked accumulation of ammonia, glutamine and alanine, and reduction in glutamate and aspartate concentrations. Administration of a subconvulsive dose of homocysteine (7.5 mmol/kg) gave rise to changes in ammonia and amino acids, qualitatively similar to those occurring during seizures. It is concluded that although changes in the metabolites of the energy reserve were mainly caused by the induced seizures, those affecting amino acid concentrations were significantly influenced by accumulation of ammonia, secondary to metabolism of injected homocysteine. Cerebral blood flow (CBF) and oxygen utilization (CMRO2) were measured during sustained seizures. CMRO2 rose to 150% of control, with a corresponding increase in CBF.     

Sex differences in the number of synaptic junctions in the binocular area of the rat visual cortex

We had found that the binocular area of the visual cortex is larger in volume and has more neurons in male than in female rats. The present study examined whether the number of synaptic junctions in this area is sexually dimorphic. Ten littermate pairs of 90-day-old (socially housed) Long-Evans hooded rats were used. Synaptic junctions were counted and their lengths were measured on electron micrographs taken from layers II–III of the binocular visual cortex. There were no sex differences in the numerical density of synaptic junctions, the number of synaptic junctions per neuron, or the length of synaptic junctions within any synaptic category or of all synapses combined. Sex differences were found in the total number of synaptic junctions and in several categories (asymmetric synapses, spine synapses, asymmetric spine synapses): male rats had more synaptic junctions than female rats because of the larger volume of layers II--III in the binocular area of male rats. These data indicate that neurons in the binocular visual cortex of both male and female rats receive a characteristic number of synaptic junctions, but the greater number of neurons in the binocular area of male rats results in more synaptic junctions in the area. © 1995 Wiley-Liss, Inc.     

Association fiber pathways to the frontal cortex from the superior temporal region in the rhesus monkey

The projections to the frontal cortex that originate from the various areas of the superior temporal region of the rhesus monkey were investigated with the autoradiographic technique. The results demonstrated that the rostral part of the superior temporal gyrus (areas Pro, Ts1, and Ts2) projects to the proisocortical areas of the orbital and medial frontal cortex, as well as to the nearby orbital areas 13, 12, and 11, and to medial areas 9, 10, and 14. These fibers travel to the frontal lobe as part of the uncinate fascicle. The middle part of the superior temporal gyrus (areas Ts3 and paAlt) projects predominantly to the lateral frontal cortex (areas 12, upper 46, and 9) and to the dorsal aspect of the medial frontal lobe (areas 9 and 10). Only a small number of these fibers terminated within the orbitofrontal cortex. The temporofrontal fibers originating from the middle part of the superior temporal gyrus occupy the lower portion of the extreme capsule and lie just dorsal to the fibers of the uncinate fascicle. The posterior part of the superior temporal gyrus projects to the lateral frontal cortex (area 46, dorsal area 8, and the rostralmost part of dorsal area 6). Some of the fibers from the posterior superior temporal gyrus run initially through the extreme capsule and then cross the claustrum as they ascend to enter the external capsule before continuing their course to the frontal lobe. A larger group of fibers curves round the caudalmost Sylvian fissure and travels to the frontal cortex occupying a position just above and medial to the upper branch of the circular sulcus. This latter pathway constitutes a part of the classically described arcuate fasciculus.