急性前循环缺血性卒中血管内治疗术后早期脑血流自动调节功能与预后关系研究

目的 使用传递函数分析（transfer function analysis，TFA）和Spearman相关性分析计算急性前循环
缺血性卒中血管内治疗术后患者早期脑血流自动调节（cerebral autoregulation，CA）功能，比较两种方
法得出的自动调节参数与临床预后的相关性。
方法 前瞻性纳入急性前循环缺血性卒中且进行了血管内治疗的患者，收集患者的影像、临床信息。
术后48 h内使用TCD联合无创动脉压，连续采集患者双侧大脑中动脉脑血流速度（flow velocity，FV）
和逐搏动脉压（arterial blood pressure，ABP）。使用TFA计算FV和ABP信号的极低频（0.02～0.07 Hz）、
低频（0.07～0.20 Hz）、高频（0.20～0.50 Hz）的相位差和增益；使用Spearman相关性分析计算平均血
流速度指数（mean flow velocity index，Mx）。根据患者90 d mRS评分分为预后良好（mRS≤2分）和预
后不良（mRS＞2分），比较不同预后患者上述CA参数的差异，并用多因素分析评估不同方法计算的CA
参数对患者90d预后的影响。另外，分析CA参数与术后7 d NIHSS评分相对术前的改善（ΔNIHSS）、90 d
mRS评分、术前梗死体积、术后48 h增加的梗死体积等临床指标的相关性。
结果 共纳入52例患者，90 d预后良好18例，预后不良34例。与预后良好患者相比，预后不良患者
Mx较高[0.40（0.18～0.50）vs 0.26（0.05～0.36），P =0.012]，但两组各频段相位差和增益的差异均
无统计学意义。Mx与术后7 d的ΔNIHSS、90 d mRS评分、术前梗死体积、术后48 h增加的梗死体积
均为正相关性（r 值分别为0.299、0.382、0.561和0.286，P值分别为0.031、0.005、<0.001和0.040），
极低频相位差与术前梗死体积、90 d mRS评分均呈负相关（r 值分别为-0.282、-0.276，P值分别
为0.043、0.048）。多因素回归分析提示Mx值是90 d预后不良的独立影响因素（OR 132.69，95%CI
5.71～3081.96，P =0.002）。
结论 急性前循环缺血性卒中血管内治疗术后早期CA功能相对保留与预后良好相关。相比于相位
差和增益，Mx与90 d临床结局有更强的相关性。     

大脑中动脉闭塞或狭窄缺血性卒中患者血液炎性标志物变化

【摘要】
目的 观察大脑中动脉闭塞（middle cerebral artery occlusion,MCAO）或狭窄的缺血性卒中患者的危险
因素及血白细胞（white blood cell,WBC）、红细胞沉降率（erythrocyte sedimentation rate,ESR）和超敏
C反应蛋白（high-sensitivity C-reactive protein,hs-CRP）的变化。
方法 2005年1月～2011年1月期间北京友谊医院神经内科连续入选符合研究标准的262例缺血性卒中
患者,其中98例MCAO（闭塞组）、23例大脑中动脉（middle cerebral artery,MCA）狭窄率70%～99%（重
度狭窄组）、60例MCA狭窄率50%～69%（中度狭窄组）和81例MCA狭窄率<50%（轻度狭窄组）。比较四
组患者的危险因素及入院24 h血WBC、ESR和hs-CRP等指标。
结果 闭塞组、重度狭窄和中度狭窄组糖尿病患病率明显高于轻度狭窄组（P分别为0.008、0.044和
0.018）,其他危险因素在四组间比较差异均无显著性。闭塞组WBC、ESR和hs-CRP水平均高于轻度狭窄
组（P分别为0.005、0.002和0.001）;重度狭窄组ESR亦高于轻度狭窄组（P =0.026）。
结论 MCA闭塞和重度狭窄的缺血性卒中患者血WBC、ESR和hs-CRP水平高于MCA轻度狭窄患者。     

软脑膜侧支循环对症状性大脑中动脉 狭窄或闭塞患者卒中复发及死亡事件影响研究

目的 通过磁共振血管成像（magnetic resonance angiography,MRA）检查,研究不同途径的软脑膜动
脉（leptomeningeal anastomoses,LMA）代偿对症状性大脑中动脉（middle cerebral artery,MCA）狭窄或闭
塞患者1年内预后的影响。
方法 选取在首都医科大学附属北京天坛医院神经内科住院治疗的症状性MCA狭窄或闭塞患者,经
过MRA评价LMA代偿情况分为大脑前动脉（anterior cerebral artery,ACA）途径代偿组、大脑后动脉
（posterior cerebral artery,PCA）途径代偿组、双代偿途径组和无代偿组,据随访结果,对不同途径
LMA代偿组预后对比,了解不同途径LMA代偿对患者预后的影响。
结果 随访1年中有17例缺血性卒中复发事件,复发率为6.83%。共6例患者死亡,死亡率为2.4%。在4
组不同途径LMA代偿组间,缺血性卒中（χ2=7.824、P =0.0497）、总的不良事件（χ2=11.238、P =0.011）
存在显著差异。其中无代偿组卒中复发高于双代偿途径组（P =0.022）。在总不良事件方面,无代偿组
与双代偿途径组、无代偿组与ACA代偿途径组之间存在显著差异,P值分别为0.004和0.04。有代偿组
在缺血性卒中、总事件等方面均低于无代偿组（P值分别为0.021和0.003）;两组间脑出血、全因死亡
等方面无显著差异。
结论 良好的LMA可以有效减少症状性MCA狭窄或闭塞患者1年内缺血性卒中等不良事件的发生,但
对脑出血及全因死亡无影响。     

脑深静脉血栓形成12例临床及影像分析

目的 探讨脑深静脉血栓形成（deep cerebral venous thrombosis,DCVT）的临床及影像学特点。
方法 回顾性分析2004年12月～2013年5月在北京协和医院神经内科住院的经数字减影血管造影
（digital subtraction angiography,DSA）或者磁共振静脉成像（magnetic resonance venography,MRV）确诊
的12例DCVT患者的临床表现、影像学特征、治疗及预后情况。
结果 12例DCVT患者中男性7例,女性5例,年龄24.5（19.75,33.5）岁。临床表现：头痛11例［11/12
（92%）］;不同程度意识障碍5例［5/12（42%）］,其中1例为昏迷;抽搐发作5例［5/12（42%）］;其
他局灶体征（单侧肢体无力）2例［2/12（17%）］。影像表现：累及直窦和大脑大静脉最多见,分别为
11例［11/12（92%）］及8例［8/12（67%）］,累及大脑内静脉3例［3/12（25%）］,基底静脉1例［1/12
（8%）］,所有患者均合并其他静脉窦受累。8例患者行头颅计算机断层扫描（computed tomography,CT）
和（或）磁共振成像（magnetic resonance imaging,MRI）检查,其中丘脑病灶4例［4/8（50%）］,基
底节区病灶2例［2/8（25%）］,额或顶叶病灶3例［3/8（38%）］,其中病灶内合并出血者2例［2/8
（25%）］。治疗预后：12例患者中除1例因感染性休克死亡,未能接受抗凝治疗外,其余11例均给予抗
凝治疗,最终症状体征基本消失,复查影像学病灶明显好转或消失。
结论 意识障碍及双侧丘脑病变是DCVT的常见临床及影像表现,需注意识别;大脑大静脉及直窦为
常见受累深静脉（窦）,且常并存其他静脉窦受累;DCVT虽急性期症状凶险,如及早诊断及治疗,预后
可相对较好。     

卒中后失语症类型及其影响因素分析

目的 通过探讨性别、年龄、病变部位及卒中病因等与失语症类型之间的关系，探索影响卒中后失
语类型的因素。
方法 回顾性分析2004年1月-2018年12月于首都医科大学附属北京天坛医院就诊、因语言障碍进行
西部失语成套测验（western aphasia battery，WAB）的卒中后失语症患者临床资料。分析失语症类型与
性别、年龄、卒中类型、卒中病因及发病机制之间的关系。
结果 共纳入失语症患者681例，按照失语症类型分为完全性失语（global aphasia，GA）（n =185）、
运动性失语（broca’s aphasia，BA）（n =148）、经皮质混合性失语（mixed transcortical aphasia，MTCA）
（n =30）、经皮质运动性失语（transcortical motor aphasia，TCMA）（n =67）、感觉性失语（werni cke’s
aphasia，WA）（n =69）、经皮质感觉性失语（transcortical sensor aphasia，TCSA）（n =21）、传导性失
语（conduction aphasia，CA）（n =32）和命名性失语（anomic aphasia，NA）（n =129）。将患者分为青年组
（18～44岁）、中年组（45～59岁）、老年组（≥60岁），校正其他因素影响后，三组人群间失语症类型
无统计学差异。男性和女性患者的失语症类型也无统计学差异。各类型失语症患者的病变部位具有
异质性，除合并经典语言区损伤外，还可合并左侧基底节及丘脑损伤。在脑出血所致的各类型失语
症患者中，最常见的病因均为高血压（77.8%～100.0%）。脑梗死后GA患者中，最常见的卒中发病机制
是混合型（42.4%）和动脉-动脉栓塞（27.3%），而BA、WA及CA患者以动脉-动脉栓塞（分别占51.5%，
71.4%和40.0%）最常见，TCMA、TCSA及NA以低灌注/栓子清除能力下降（分别占65.9%，58.3%和
38.4%）最常见。
结论 年龄及性别对失语症类型均无明显影响。男性和女性患者均以GA、BA和NA最为常见。病变
部位对失语症类型具有重要影响，卒中病因及发病机制对失语症类型的影响可能与特定血管及血管
供血区损伤有关。     

儿童缺血型烟雾病的临床和影像分析

【摘要】
目的 分析儿童缺血型烟雾病患者的临床和影像特点,探讨脑梗死的相关因素。
方法 回顾性分析2011年6月～2012年6月收治的27例儿童缺血型烟雾病患者的临床及影像学资料。
大脑半球分为无脑梗死半球32侧和脑梗死半球22侧,将患者性别、年龄、造影特点（包括54侧半球
的Suzuki分期、大脑后动脉分期,眼动脉、颞浅动脉、脑膜动脉、枕动脉、上颌动脉和后循环向前循
环代偿）与脑梗死的发生进行统计分析。
结果 27例患者的临床资料显示性别和年龄与脑梗死的发生差异不具有显著性（性别χ2=2.095,
P =0.148;年龄χ2=4.286,P =0.453）。根据半球计算：皮质脑梗死17侧（17/22）,额叶梗死14侧
（14/22）,皮质下脑梗死9侧（9/22）。无梗死侧半球和梗死侧半球Suzuki分期以及大脑后动脉分期
的差异具有显著性（Suzuki分期Z=－3.054,P =0.002;大脑后动脉分期Z=－4.557,P <0.001）。眼动脉、
颞浅动脉、脑膜动脉、枕动脉、上颌动脉和后循环向前循环代偿与脑梗死的发生差异不具有显著性。
结论 本研究显示儿童缺血型烟雾病皮质脑梗死较皮质下脑梗死常见。在皮质脑梗死中,额叶脑
梗死最常见。脑梗死的发生与Suzuki分期和大脑后动脉受累程度有关。     

酒精对缺血-再灌注大鼠脑组织的保护作用

【摘要】
目的 探讨酒精对缺血-再灌注大鼠脑组织梗死面积、皮质凋亡诱导因子（apoptosis induced factor,
AIF）及缺氧诱导因子-1α（hypoxia induced factor-1α,HIF-1α）表达的影响。
方法 将54只健康雄性Wistar大鼠随机分为3组,分别为假手术组、缺血-再灌注组（对照组）、缺
血-再灌注后酒精治疗组（治疗组）。以改良线栓法制成大鼠大脑中动脉闭塞（middle cerebral artery
occlusion,MCAO）模型,2 h后拔出线栓,形成缺血-再灌注,治疗组立即腹腔注射1.5 g/kg酒精（无水
酒精稀释成50%酒精）,对照组与假手术组腹腔注射等剂量的生理盐水。观察大鼠脑梗死灶面积的
大小,采用免疫组化方法检测大鼠缺血-再灌注脑组织AIF及HIF-1α的表达。
结果 治疗组大鼠脑梗死面积较对照组明显减小［（35.33 6.06）mm2 vs （55.50 3.62）mm2,
P <0.001］;对照组大鼠脑皮质区AIF及HIF-1α表达分别为（36.75 8.99）个/HP和（49.25 12.04）
个/HP;治疗组大鼠脑皮质区AIF及HIF-1α表达分别为（20.75 7.46）个/HP和（70.25 11.12）个/HP;
治疗组大鼠脑皮质区AIF的表达明显低于对照组（P <0.001）,而HIF-1α的表达明显高于对照组
（P <0.001）。
结论 1.5 g/kg酒精对缺血-再灌注大鼠脑组织具有保护作用,可能是通过减少细胞凋亡而减轻脑
损伤。     

三维动脉自旋标记评价丁苯酞注射液对急性缺血性卒中患者脑血流的影响

目的 采用MRI 三维动脉自旋标记（3-dimensional arterial spin labeling，3D-ASL）技术观察急性缺血
性卒中患者使用丁苯酞注射液对脑血流灌注的影响。
方法 纳入60例非大动脉狭窄或闭塞性急性缺血性卒中患者，随机分为观察组（30例）和对照组
（30例）。对照组采用常规治疗，观察组在对照组治疗基础上加用丁苯酞注射液，疗程为14 d。治疗前
后均进行头颅3D-ASL检查来测量梗死灶相对脑血流量（relative cerebral blood flow，rCBF）的变化。
结果 观察组和对照组治疗前rCBF差异无统计学意义，治疗后观察组rCBF高于对照组（0.97±0.45
vs 0.35±0.15，P =0.003）。
结论 丁苯酞注射液可以提高急性缺血性卒中患者梗死病灶区域的脑血流灌注水平。     

特发性高颅压患者脑血流自动调节研究

目的 分析特发性颅内压增高（idiopathic intracranial hypertension，IIH）患者脑血流自动调节机能。
方法 连续入组2018年12月-2019年3月在首都医科大学附属北京天坛医院就诊的IIH患者，并选取年
龄匹配的健康志愿者作为对照组。应用传递函数的算法分析TCD显示的大脑中动脉血流速度及动脉
血压的自然波动以评估脑血流自动调节机能。
结果 入组IIH组10例，对照组13例。所有入组者均完成了双侧大脑半球的脑血流自动调节检测，共
检测了20个高颅压半球及26个正常对照半球。与对照组相比，IIH组大脑中动脉脑血流增益显著降
低[（0.64±0.35）%/% vs（0.37%±0.20）%/%，P =0.004]；相位也显著降低（58.80±20.86°vs
39.16±23.79°，P =0.005），差异有统计学意义。IIH组每秒钟脑血流速度的恢复率较对照更低，但差
异尚未达到统计学意义（[ 26.34±43.29）%/s vs（38.81±20.16）%/s，P=0.240]。
结论 IIH患者脑血流自动调节机能显著受损。     

大剂量高压氧超早期治疗对局部脑梗死大鼠细胞凋亡的影响

目的 观察大剂量高压氧（hyperbaric oxygenation,HBO）超早期治疗对永久性大脑中动脉阻塞
（middle cerebral artery occlusion,MCAO）大鼠细胞凋亡的影响。
方法 制作SD大鼠永久性MCAO模型,随机分为对照组（n =36）和HBO组（n =36）,HBO组大鼠于模型
制备成功后3 h予单次9 h HBO治疗,压力0.2 MPa。于模型成功后3 h、13 h、72 h,行大鼠Garcia神经功
能评分,于13 h、72 h分别将大鼠脑组织进行2,3,5苯四氮唑（tetrazolium chloride,TTC）染色测定梗
死容积百分比,应用脱氧核糖核苷酸末端转移酶介导的缺口末端标记法（terminal-deoxynucleotidyl
transferase mediated nick end labeling,TUNEL）检测细胞凋亡,流式细胞仪检测线粒体膜电位。
结果 ①两组大鼠在MCAO 13 h时（P均=0.007）和72 h时（P均＜0.001）均较同组MCAO 3 h时神经功
能明显改善,但各时间点两组间神经功能无显著差异。②13 h时,两组大鼠脑梗死容积比无显著差异;
72 h时,对照组大鼠脑梗死容积比较13 h时增大（P =0.02）,而HBO组无显著变化,HBO组较对照组脑
梗死容积比小（P =0.02）。③HBO组及对照组在13 h、72 h均可见凋亡细胞,13 h时HBO组凋亡细胞数少
于对照组（P =0.04）。④大鼠MCAO后线粒体膜电位降低,HBO组在13 h、72 h的线粒体膜电位均高于对
照组,差异有显著性（P均＜0.001）。
结论 大剂量HBO超早期治疗可缩小大鼠脑梗死容积,抑制线粒体膜电位降低,进而减少细胞凋亡
可能是高压氧治疗脑梗死的机制之一。     

瓦氏动作在脑血流自动调节功能中的应用

CA是指脑血流在动脉血压和脑灌注压发生改变时保持相对稳定的一个复杂的多因素过 程。脑血流自动调节与多种神经系统疾病如脑血管病、帕金森病、头痛、自主神经功能障碍等疾病的 发生、发展及临床预后相关。对脑血流自动调节功能有很多种评估测量方法，监测瓦氏动作所诱导 的血压变化更具有操作性及标准化，适用于各种人群，其安全、简单、准确的特点使其在脑血流自动 调节中运用十分广泛。本文重点对瓦氏动作在脑血流自动调节功能中的应用做一个综述介绍。     

Monitoring of Cerebrovascular Autoregulation: Facts, Myths, and Missing Links

The methods for continuous assessment of cerebral autoregulation using correlation, phase shift, or transmission (either in time- or frequency-domain) were introduced a decade ago. They express dynamic relationships between slow waves of transcranial Doppler (TCD), blood flow velocity (FV) and cerebral perfusion pressure (CPP), or arterial pressure (ABP). We review a methodology and clinical application of indices useful for monitoring cerebral autoregulation and pressure-reactivity in various scenarios of neuro-critical care. Facts: Poor autoregulation and loss of pressure-reactivity are independent predictors of fatal outcome following head injury. Autoregulation is impaired by too low or too high CPP when compared to autoregulation with normal CPP (usually between 60 and 85 mmHg; and these limits are highly individual). Hemispheric asymmetry of the bi-laterally assessed autoregulation has been associated with asymmetry of CT scan findings: autoregulation was found to be worse ipsilateral to contusion or lateralized edema causing midline shift. The pressure-reactivity (PRx index) correlated with a state of low CBF and CMRO₂ revealed using PET studies. The PRx is easier to monitor over prolonged periods of time than the TCD-based indices as it does not require fixation of external probes. Continuous monitoring with the PRx can be used to direct CPP-oriented therapy by determining the optimal CPP for pressure-reactivity. Autoregulation indices are able to reflect transient changes of autoregulation, as seen during plateau waves of ICP. However, minute-to-minute assessment of autoregulation has a poor signal-to-noise ratio. Averaging across time (30 min) or by combining with other relevant parameters improves the accuracy. Myths: It is debatable whether the TCD-based indices in head injured patients can be calculated using ABP instead of CPP. Thresholds for functional and disturbed autoregulation dramatically depends on arterial tension of CO₂—therefore, comparison between patients cannot be performed without comparing their PaCO₂. The TCD pulsatility index cannot accurately detect the lower limit of autoregulation. Missing Links: We still do not know whether autoregulation-oriented therapy can be understood as a consensus between CPP-directed protocols and the Lund-concept. What are the links between endothelial function and autoregulation indices? Can autoregulation after head injury be improved with statins or EPO, as in subarachnoid hemorrhage? In conclusion, monitoring cerebral autoregulation can be used in a variety of clinical scenarios and may be helpful in delineating optimal therapeutic strategies.     

出血性卒中的脑血流自动调节研究进展

脑血流自动调节 （cerebral autoregulation, CA） 是人体在一定血压或脑灌注压波动范围内维持脑血流量 （cerebral blood flow） 相对稳定的能力, 可避免脑组织发生高灌注或低灌注。 CA在出血性卒中中存在不同程度受损, 且与临床因素及预后密切相关。 对出血性卒中患者行CA监测不仅可评估临床预后, 还可为动脉血压及脑灌注压的管理提供参考信息。 本文主要就脑出血 （intracerebral hemorrhage, ICH） 和蛛网膜下腔出血 （subarachnoid hemorrhage, SAH） 的CA相关进展做一综述, 旨在探讨CA在上述疾病中的改变及其临床应用价值。     

Transcranial Doppler for evaluation of cerebral autoregulation

Transcranial Doppler ultrasound (TCD) can measure cerebral blood flow velocity in the main intracranial vessels non-invasively and with high accuracy. Combined with the availability of non-invasive devices for continuous measurement of arterial blood pressure, the relatively low cost, ease-of-use, and excellent temporal resolution of TCD have stimulated the development of new techniques to assess cerebral autoregulation in the laboratory or bedside using a dynamic approach, instead of the more classical ‘static’ method. Clinical applications have shown consistent results in certain conditions such as severe head injury and carotid artery disease. Studies in syncopal patients revealed a more complex pattern due to aetiological non-homogeneity and methodological limitations mainly due to inadequate sample-size. Different analytical models to quantify autoregulatory performance have also contributed to the diversity of results in the literature. The review concludes with specific recommendations for areas where further validation and research are needed to improve the reliability and usefulness of TCD in clinical practice.     

Change in cerebral autoregulation as a function of time in children after severe traumatic brain injury: a case series

Objective The objective of this study was to describe changes in cerebral autoregulation after severe pediatric traumatic brain injury (TBI). Materials and methods Two cerebral autoregulation tests were performed during the first 10 days after severe TBI in children <16 years. Cerebral autoregulation was quantified using the mean autoregulatory index (mARI). Results Nine (five males/four females) children (10 ± 5 years) with severe (admission Glasgow Coma Scale (GCS), 5 ± 2) TBI were enrolled. Thirty (3/9) percent of initial exams revealed impaired cerebral autoregulation; all three had returned to intact cerebral autoregulation on second exam. However, in three of nine (33%) patients, cerebral autoregulation worsened on second exam. Of the factors examined, worsening mARI on second exam was associated with worsening head computed tomography (CT) lesion. Conclusions Cerebral autoregulation often changed and worsened during the first 9 days after severe pediatric TBI. Worsening cerebral autoregulation may mirror worsening TBI.     

Transfer function analysis of dynamic cerebral autoregulation: A white paper from the International Cerebral Autoregulation Research Network

Cerebral autoregulation is the intrinsic ability of the brain to maintain adequate cerebral perfusion in the presence of blood pressure changes. A large number of methods to assess the quality of cerebral autoregulation have been proposed over the last 30 years. However, no single method has been universally accepted as a gold standard. Therefore, the choice of which method to employ to quantify cerebral autoregulation remains a matter of personal choice. Nevertheless, given the concept that cerebral autoregulation represents the dynamic relationship between blood pressure (stimulus or input) and cerebral blood flow (response or output), transfer function analysis became the most popular approach adopted in studies based on spontaneous fluctuations of blood pressure. Despite its sound theoretical background, the literature shows considerable variation in implementation of transfer function analysis in practice, which has limited comparisons between studies and hindered progress towards clinical application. Therefore, the purpose of the present white paper is to improve standardisation of parameters and settings adopted for application of transfer function analysis in studies of dynamic cerebral autoregulation. The development of these recommendations was initiated by (but not confined to) the Cerebral Autoregulation Research Network (CARNet – www.car-net.org).     

One-Minute Dynamic Cerebral Autoregulation in Severe Head Injury Patients and its Comparison with Static Autoregulation. A Transcranial Doppler Study

Objective  To compare dynamic and static responses of cerebral blood flow to sudden or slow changes in arterial pressure in severe traumatic brain injury (TBI) patients. Design  Prospective study. Patients and Methods  We studied 12 severe TBI patients, age 16–63 years, and median GCS 6. We determined the dynamic cerebral autoregulation: response of cerebral blood flow velocity to a step blood pressure drop, and the static cerebral autoregulation: change in cerebral blood flow velocity after a slow hypertensive challenge. Results  During the dynamic response, the median drop in arterial pressure was 21 mm Hg. Dynamic response was graded between 9 (best) and 0 (worst). The median value was 5; four patients showed high values, (8–9), five patients showed intermediate values (4–6). In three patients (value = 0), the CBFV drop was greater than the cerebral perfusion pressure drop, and maintained through 60 s. The static cerebral autoregulation was preserved in 6/11 patients. The comparison between the two showed four different combinations. The five patients with impaired static cerebral autoregulation showed unfavorable outcome. Conclusions  A sharp dynamic vasodilator response could not be sustained, and a slow or absent reaction to a sudden hypotensive challenge could show an acceptable cerebral autoregulation in the steady state. We found that patients with impaired static cerebral autoregulation had a poor outcome, whereas those with preserved static cerebral autoregulation experience favorable outcomes.     

Hemispheric Differences in Cerebral Autoregulation in Children with Moderate and Severe Traumatic Brain Injury

Introduction  To examine hemispheric differences in cerebral autoregulation in children with traumatic brain injury (TBI). After IRB approval and consent, subjects underwent static cerebral autoregulation testing during the first 9 days after PICU admission. Cerebral autoregulation was quantified using the autoregulatory index (ARI). Results  Forty-two (27 M:15 F) children (10 ± 5 years) with TBI and admission Glasgow coma scale score (5 ± 2) were enrolled. Seven (54%) of the 13 children with focal TBI and 8 (28%) of 29 children with diffuse TBI had impairment or absence of cerebral autoregulation of atleast one hemisphere. In patients with isolated focal TBI, ARI was lower (0.40 ± 0.40 vs. 0.67 ± 0.40; P = 0.03) in the side of TBI than in the unaffected hemisphere, but cerebral autoregulation was often impaired on the side without TBI or shift (5/13) on head CT. There was no difference in ARI between hemispheres in children with diffuse TBI, with or without superimposed focal lesions (P = 0.17). Patients with bilateral intact cerebral autoregulation tended to have higher 6 month Glasgow Outcome Score (GOS) than patients with either unilateral or bilateral cerebral autoregulation impairment (GOS 4.0 ± 0.60 vs. 3.6 ± 0.80; P = 0.08). Conclusions  Hemispheric differences in cerebral autoregulation were common in children with isolated focal TBI. Absence of TBI on CT was not always associated with intact cerebral autoregulation. Patients with bilaterally intact cerebral autoregulation tended to have better outcomes.     

Dynamics of cerebral blood flow autoregulation in hypertensive patients

In hypertensive patients, the upper and lower limits of cerebral autoregulation are shifted to higher levels. However, the dynamics of cerebral autoregulation in hypertensive patients are less well known. We compared the dynamics of cerebral autoregulation in 21 treated hypertensive patients (13 men and 8 women; mean age: 48.9+/-13.6 years) and in 21 normotensive subjects (13 men and 8 women; mean age: 51+/-14.5 years) by transcranial Doppler (TCD) of the middle cerebral artery (MCA) during the acute decrease in blood pressure induced by standing up after 2 min in squatting position. MCA maximal outline blood flow velocity (FV), blood pressure (Finapres) and end-tidal PCO2 were continuously monitored and computerised. A cerebral vascular resistance index (CR) was calculated as follows: mean arterial BP/MCA mean FV with normalised changes in CR per second during the blood pressure decrease (CR slope). The CR slope reflecting the rate of cerebral autoregulation did not differ between the two groups and within the hypertensive patients [well controlled (8 patients) and not controlled (13 patients)]. The time to maximum decrease of CR (T1) and the time to full recovery of CR after the initial drop (T2) were also similar in the two groups (controls T1: 11.3+/-3.1 s, T2: 12+/-5.9 s; hypertensive T1: 11.7+/-2.5 s, T2: 10.7+/-4.5 s) and within hypertensive patients. These findings suggest that the dynamics of cerebral autoregulation are well preserved in hypertensive patients, with no difference according to the efficiency of treatment of hypertension.     

脑血流自动调节范围内维持脑血流恒定的因素

目的探讨脑血流自动调节范围内稳定脑血流速度的血流动力学因素。方法利用经颅多普勒检测SD大鼠大脑中动脉的血流速度(cerebral blood flow velocity,CBFV),并同步记录有创动脉血压,绘制自动调节曲线,判断脑血流自动调节上、下限。计算临界关闭压(critical closing pressure,CCP)和血管面积阻力指数(resistance area product,RAP)。分析CCP、RAP与平均动脉压(mean artery blood pressure,MABP)之间的关系。结果动脉血压升高或降低过程中,正常大鼠脑血流自动调节上、下限分别为148.12±7.49 mm Hg、62.96±3.34 mm Hg。脑血流自动调节范围内,CBFV随动脉血压改变轻微(每10 mm Hg MABP,升压:0.65±0.27 cm/s;降压:0.43±0.23 cm/s),而CCP和RAP则随动脉血压明显改变(每10 mm Hg MABP,升压:4.60±1.06 mm Hg、0.11±0.04mm Hg;降压:6.74±0.59 mm Hg、0.09±0.02 mm Hg)。虽然CBFV、CCP、RAP的变化都与MABP相关,但控制CBFV的变动后,CCP和RAP随MABP改变相关性更加明显,其中CCP的变化幅度以及与MABP的相关性明显大于RAP(升压:Beta=0.561、0.418;降压:Beta=0.694、0.266,P均=0.000)。结论大鼠脑血流自动调节有效范围内,脑血流的稳定主要通过CCP和RAP改变对抗动脉血压的变动而实现,尤其是CCP相应升高或降低。