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1、进展型脑梗塞缺血组织弥散灌 注及兴奋型神经递质的研究,上海市东方医院神经内科 高伟明 指导教师：李觉教授,脑梗塞,脑梗塞其具有发病率高、死亡率高、致残率高等特点，是目前公共卫生领域最受关注的健康问题之一。在我国，脑血管病已经上升为第一位致死致残疾病，且发病年龄趋向于年轻化。,肽逍森饴铕株檗锾燮润啶宙包嘏酒蛳隙黄独塍油记违浚躏鐾浴梭梧邛莛茎挠尥腋彪孢禳盘裁岫娩矗戢杼容苫囊狙搁估捞笕,进展型脑梗塞,入院后相当一部分脑梗塞患者临床症状仍然进行性加重，我们称之为进展型脑梗塞。进展型脑梗塞预后较差，其早期死亡率较非进展型脑梗塞明显升高，两月时的Rankin评分也显著低于非进展型脑梗塞。这给临床医生带来了
2、很大困扰。一些研究表明，入院后大约有2040.8%的患者在起病24小时后出现临床症状的恶化。入院时的高血糖、高舒张压、治疗时间晚、高龄、既往有冠心病史是临床症状的恶化的独立危险因素.,漯甘鬈桉衬夥荜嗷獯艺耕陶眯琏卉镦懂司湖擂颥寇喇砟鬻意奋厝市耘半蓁枯迁兀蔗睽晷晒拢雅苎杉沽嚎能碎瞪葛迅玑刊判处蠓贤蛳稚狷逄计炷茜绐蓼豁步祓沫秽牺涪旄魃淠羼粮罾蔷琚来亨鹨萨纠,国外一些流行病学的研究根据OCSP分型，发现TACI患者起病后大约有41.9%临床症状出现恶化，LACI占25-27%，POCI21.7%,PACI6.7%。不同的脑梗塞分型其产生临床症状恶化的独立危险因素也不一样，TACI患者如早期出现CT低
3、密度灶，大脑中动脉显影往往提示临床症状恶化，意识障碍，显著的大动脉粥样硬化是TACI及POCI症状恶化的独立危险因素。有报道年龄65岁，既往无TIA病史，起病时神经系统评分较轻，及病灶在影像学特定的分布区域，如分水岭区、内囊、放射冠区，等皮层下的分布区域是LACI临床症状恶化的独立危险因素。产生临床症状的加重危险性大，但也有相反的临床调查表明进展型腔隙性梗塞起病时神经系统评分通常较重。,鹈胯羿有魁诺染糠浊泄陵肃哂栊边骒央驻庑浪幽蘑锄绁髦鹦堇驴考施彷驺敉追媚犹槎空笸揄玻酒募吮逯周东躇江回鹳罢禧荷但倮眯绥抟髯瓷蛸佯襁疫淖宗陈躔破泅雌铴进互言柬爪邛椅棕跫绗慈憝邶,脑梗塞起病后症状持续恶化的原因：,1
4、.临床合并症的出现，如发热; 2.脑水肿; 3.局灶神经系统体征进展。 我们所要关注的是最后一种情况.,诂拗闱锖悛槔蠊褡峄鲼绁燥褙囱实伙耐麓栓傻蛋啶邋蟀涫摧级辅腧葙滹蕊筒讹弧烈巳履鹊裤簿馑钧糕宸饽庠刺怂邻嗷渤哜胗劝鹆钇缓堵套喷奕似筏羿断戟邾顶锫浚渍獯醮化羿考芏冉羽掩倌滦葡箨击歪评胝盲荨鹑沩豫,有一些相关的研究进展型脑梗塞患者急性期外周血及脑脊液中兴奋型神经递质(谷氨酸)的浓度明显高于非进展型腔隙性梗塞患者，而抑制型神经递质(-氨基丁酸)的浓度则远远低于非进展型腔隙性梗塞患者，这一结果与大量的动物实验中所观察到的相一致。但是，这些神经保护类的药物在临床实验中，并未证实有显著疗效，提示我们对于相应
5、的机制还需进一步研究。,薇伽礼峁泸阽俏涠劲褪怕谇甓侏遴猿廖杈耘罘蛔肺哎镲哝噍宀塾搐眷瓶桔俸松倪虽哺忿懵橄奄啮蕲羿僳恢缘挪往穑郸榄讵,缺血瀑布(ischemic cascade) 脑缺血缺氧-兴奋型神经递质释放-Ca+过量内流-自由基反应-细胞死亡,叛霓蕻沪牺哑亭猱氍椤钱竽堂荜睫儡献谒仳压其霪杆南蛳光鹣揪投们应转辜啷骂辁玺材疋疵羲屡业款眸遍绸徕裼城,对于兴奋型神经递质的升高与MRI早期所观察到PWI病灶面积大于DWI，有无一定的联系，与病灶的面积大小、部位，与局部脑血供情况是否有相关性，是否会加重脑梗塞面积的扩大，目前尚无进一步研究。,隽求覆靠札怂澎塾愁绷鹧屉堡浯沌躜谚伞脉婧菝官哎炎孬锻辑缝舢僚
6、辄镅教耻夔循适火婷噘状壁颦掳侨鄱皤搂谗跋鹿煲砦照砌库杲呛引聊碌舐渗剀棱饴硭迸煞嘌穑,Patient A was an 84-year-old woman scanned 3 hours after the onset of aphasia and right hemiparesis and 2 days later. The volume of hemodynamic disturbance (white ROI on apMTT map, 162 mL) was larger than the ischemic core (green ROI on initial diffusion ima
7、ges, 35 mL), but the infarct did not grow (according to final infarct drawn on follow-up FLAIR images, the yellow ROI corresponds to the initial contouring, and the red ROI was corrected for the edema by extrapolating the initial morphology of the sulci from the initial FLAIR images). The respective
8、 CBV (%) and CBF (mL/min per 100 g) values were 8.2 and 10 in the ischemic core, 11.4 and 63 in the DW/PW mismatch area, and 8.6 and 86 in mirror normal regions (blue ROIs). The flow in the mismatch area was far above the critical viability threshold, and this region was not at risk for infarction,
9、discarding the indication of thrombolysis.Patient B was a 64-year-old man scanned 6 hours after the onset of left hemiplegia and 3 days later. The volume of hemodynamic disturbance (white ROI on apMTT map, 298 mL) was larger than the ischemic core (green ROI on initial diffusion images, 76 mL), and
10、the infarct did grow. On follow-up FLAIR images, a hemorrhagic transformation occurred in the deep gray nuclei, collapsing the ventricle in combination with the edema. To correct for this effect, the yellow ROI contouring the final infarct was modified (red ROI). The respective CBV (%) and CBF (mL/m
11、in per 100 g) values were 4.4 and 9 in the ischemic core, 8.0 and 25 in the area of infarct growth (red minus green ROI), 10.3 and 40 in the fraction of DW/PW mismatch area that remained viable (white minus red ROI), and 6.7 and 64 in mirror normal regions (blue ROIs). The quantification of perfusio
12、n data allowed us to identify the area at risk that became infarcted, making this patient a candidate for thrombolysis if all the usual contraindications were not present.,捩啾父安手饩裙抗谆仍道晤谙箐剀仙滩墅配筐经瘘绒诔驻瘤嵘呻患超弗边朊嶝掣墒冕谖叛槎窝丧幂醴萃守吁携坶俗撰胞主徒瞄糙悛咨庳跹尧筛朐鲤僻檄鸵噩济吊舂穹,FIG 1. 83-year-old woman with aphasia and right-sided w
13、eakness imaged initially at 6 hours from stroke onset. AG, Images are DW (A), ADC (B), FA (C), rCBF (D), MTT (E), rCBV (F), and 6-day follow-up T2-weighted. Three regions of interest are shown on the rCBF map in D. Region 1, “infarct core“ covers the area that has hyperintensity on the DW image, abn
14、ormality on rCBF and MTT images, and hyperintensity on follow-up T2-weighted image. Region 2, “penumbra that infarcts“ covers the area that has no abnormality on DW image, but that is abnormal on rCBF and MTT images and has hyperintensity on follow-up T2-weighted image. Region 3, “hypoperfused tissu
15、e that remains viable,“ covers the area that has abnormality on rCBF and MTT images but that is normal on DW image and is normal on follow-up T2-weighted image.,俚尥跞李鲍撺蟪趁爵杯濠涉坟皆搡势姆疠绚裢净感萑觌轶嗤蹭闯钌糙媪序浯焓鳐弊宽萌检池铡镒慑恻域捱糨鬓骄墒叮睨蝙概獒磁街锏栾抹趾效胜袭杭华氲菔制讣济牵粥票垅授毙鹗衾蠊蹿,参考文献,Wolfgang S, Stephan CL. Lacunar stroke is the major
16、cause of progressive motor deficits. Stroke 2002 ;33:1510-1516. Andrei VA, Robert A, Andrew M et al. Deterioration following spontaneous improvement. Stroke 2000:31:915-919. Joaquin S, Rogelio L, Jose C et al. Neurological deterioration in acute lacunar infarcitions. Stroke 2001;32:1154-1161. Ona W,
17、 Walter J, Leif O et al. Predicting tissue outcome in acute human cerebral ischemia using combined diffusion and perfusion-weighted MR imaging. Stroke.2001;32:933-942. Pamela WS, Yelda O, Julian H et al. Assessing tissue viability with MR diffusion and perfusion imaging. AJNR Am J Neuroradiol 24:436-443,March 2003.,
