馮 瑞 沈龍山 劉振生 李 澄
急性腦梗死磁共振液體衰減反轉(zhuǎn)恢復(fù)序列高信號血管征機(jī)制
馮 瑞1沈龍山2劉振生3李 澄3
目的與血管造影對照探討急性腦梗死磁共振液體衰減反轉(zhuǎn)恢復(fù)序列(fluid-attenuated inversion recovery,F(xiàn)LAIR)大腦中動(dòng)脈高信號血管征(hyperintense vessel sign, HVS)的形成機(jī)制。方法回顧性分析15例急性大腦中動(dòng)脈閉塞6 h內(nèi)患者的磁共振FLAIR序列及血管造影圖像,并以血管造影分析其血流動(dòng)力學(xué)特征。結(jié)果15例急性大腦中動(dòng)脈閉塞患者HVS出現(xiàn)率為100%,頸內(nèi)動(dòng)脈造影及微導(dǎo)管局部造影顯示M1段充盈缺損,M1段以遠(yuǎn)側(cè)支逆流顯影、造影劑滯留。結(jié)論急性腦梗死HVS形成的機(jī)制可能為近端血管內(nèi)血栓形成,遠(yuǎn)端血流緩慢的側(cè)枝循環(huán)。
腦梗死;核磁共振;血管高信號;血管造影
急性缺血性卒中患者磁共振成像(magnetic resonance imaging,MRI)液體衰減反轉(zhuǎn)恢復(fù)序列(fluid-attenuated inversion recovery,F(xiàn)LAIR)大腦中動(dòng)脈呈高信號血管征(hyperintense vessel sign,HVS),但有關(guān)HVS形成的確切機(jī)制仍不清楚[1-2]。本文與腦血管造影對照,探討其形成機(jī)制及其臨床價(jià)值。
1.1 一般資料
回顧性分析腦血管造影及核磁共振掃描資料齊全的急性大腦中動(dòng)脈閉塞患者15例,其中男9例,女6例,年齡45~78歲,平均(67.5±1.2)歲。患者臨床表現(xiàn)包括對側(cè)運(yùn)動(dòng)和感覺障礙、同向偏盲和/或高級功能障礙。
1.2 檢查方法
采用GE 1.5 T Signa EXCITE II 或Siemens MAGNETOM Verio 3.0T超導(dǎo)磁共振掃描儀,頭頸聯(lián)合線圈。掃描序列包括常規(guī)MR平掃、擴(kuò)散加權(quán)成像(diffuse weighing imaging,DWI)及MRA掃描。均行常規(guī)腦血管造影及微導(dǎo)管行局部腦血管造影,明確血管阻塞的部位和范圍,側(cè)支循環(huán)情況。
15例急性腦梗死患者M(jìn)RA均表現(xiàn)為右(7例)或左側(cè)(8例)大腦中動(dòng)脈M1段閉塞,DWI上均可見大小不等高信號區(qū),最常見于外側(cè)裂區(qū)(M2、M3段),發(fā)生率為100%(15/15),M1段為93%(14/15),M4段為67%(10/15),均表現(xiàn)為不同程度點(diǎn)狀或線狀高信號。
患側(cè)頸內(nèi)動(dòng)脈造影均見大腦中動(dòng)脈M1段完全閉塞,無大腦中動(dòng)脈閉塞段以遠(yuǎn)呈不同程度逆向血流,未見充盈缺損表現(xiàn)。
Cosnard等[3]于1999年首次報(bào)道腦梗死患者的MRI FLAIR序列發(fā)現(xiàn)了顱內(nèi)血管異常高信號,之后的一系列文獻(xiàn)也相繼證實(shí)腦梗死患者FLAIR序列存在動(dòng)脈血管異常高信號,并將此異常高信號命名為HVS。其主要影像學(xué)表現(xiàn)為急性缺血性腦血管病患者中,MRI FLAIR序列上鄰近腦皮質(zhì)表面的蛛網(wǎng)膜下腔內(nèi)為腦脊液環(huán)繞的蛇紋狀或點(diǎn)狀的高信號。
關(guān)于HVS的確切發(fā)生機(jī)制目前仍不十分清楚。Sanossian 等[4]通過與血管造影對照研究認(rèn)為,HVS形成主要由于近端血管閉塞,軟腦膜側(cè)支逆向緩慢血流代償所致。閉塞遠(yuǎn)端血管由于血流動(dòng)力學(xué)的改變,在FLAIR序列上流空效應(yīng)喪失,在低信號腦脊液的對比下呈高信號。本組15例超急性期腦梗死患者血管造影術(shù)中發(fā)現(xiàn),所有大腦中動(dòng)脈閉塞患者均存在不同程度來自大腦前動(dòng)脈軟腦膜支代償。以微導(dǎo)管通過血栓后造影均發(fā)現(xiàn)血栓范圍較小,大腦中動(dòng)脈M1段遠(yuǎn)端血流緩慢,造影劑滯留,但多無明顯充盈缺損表現(xiàn)[5]。
HVS作為閉塞性腦血管病一種特殊的影像學(xué)標(biāo)志,具有重要的臨床價(jià)值。對于急性腦梗死患者,HVS結(jié)合DWI可用于缺血半暗帶的評估。有學(xué)者研究證實(shí),在DWI高信號以外的HVS區(qū)存在顯著腦灌注的異常,HVS與DWI錯(cuò)配區(qū)可視為缺血半暗帶[6]。HVS代表缺血區(qū)側(cè)枝循環(huán)的形成,對于評估患者卒中急性期病情和預(yù)后具有重要作用。HVS的出現(xiàn)與急性前循環(huán)血管閉塞患者腦梗死范圍緩慢進(jìn)展有關(guān),即此類患者可以獲得相對較長時(shí)間窗的治療機(jī)會(huì)[7-8]。
總之,本研究結(jié)合相關(guān)文獻(xiàn)提示,HVS是急性腦梗死患者特征性MRI表現(xiàn),其形成機(jī)制為血流緩慢及血栓形成共同參與。
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Formation Mechanism of HVS Based on Magnetic Resonance FLAIR Sequence for Acute Cerebral Infarction Patients
FENG Rui1SHEN Longshan2LIU Zhensheng3LI Cheng31 Radiology Department,F(xiàn)enjinting Hospital of Sihong County,Sihong 223900,China,2 Radiology Department,The Second Affiliated Hospital of Bengbu Medical College, 233040 Bengbu,China,3 Radiology Department,The First People's Hospital of Yangzhou City,Yangzhou 225001,China
Objective To discuss the HVS formation mechanism based on magnetic resonance FLAIR sequence and angiography for acute cerebral infraction patients.MethodsWithin 6 h,15 cases of acute middle cerebral artery occlusion received magnetic resonance FLAIR sequence and angiography images. The hemodynamic characteristics was analyzed based on angiography.ResultsFor 15 cases of acute middle cerebral artery occlusion,the incidence of HVS was 100%. According to the internal carotid artery angiography and micro catheter local angiography,the filling defect was presented at M1 segment. The collateral M1 segment had the countercurrent imaging and retention of contrast medium.ConclusionFor acute cerebral infraction patients,the formation mechanism of HVS may be attributed to the proximal intravascular thrombosisand slow collateral circulation of distal blood flow.【Key words】Cerebral Infraction,NMR,Hyperintense Vessel,Angiography
R743
A
1674-9316(2015)30-0157-02
10.3969/j.issn.1674-9316.2015.30.117
1 223900 江蘇省泗洪縣分金亭醫(yī)院放射科
2 233040 安徽省蚌埠市蚌埠醫(yī)學(xué)院第二附屬醫(yī)院放射科
3 225001 揚(yáng)州市第一人民醫(yī)院放射科