孛茹婷,姬廣海,鄭義,劉嶺嶺,吳玉華,楊文君,陳志強(qiáng)*
1H-MRS和臨床相關(guān)因素在新生兒腦白質(zhì)彌漫性高信號(hào)診斷中的應(yīng)用價(jià)值
孛茹婷1,姬廣海1,鄭義1,劉嶺嶺2,吳玉華3,楊文君4,陳志強(qiáng)2*
投稿日期:2015-08-19
接受日期:2015-10-05
目的 運(yùn)用單體素氫質(zhì)子波譜技術(shù)(1H-MRS)觀察新生兒腦白質(zhì)彌漫性高信號(hào)(DEHSI)成像特點(diǎn),探討DEHSI的演變規(guī)律及診斷價(jià)值。材料與方法 對(duì)95名新生兒運(yùn)用點(diǎn)分辨波譜序列對(duì)其腦組織興趣區(qū)所得代謝數(shù)據(jù)進(jìn)行分析研究。結(jié)果 生后年齡、胎齡、頭圍均與DEHSI評(píng)估之間呈顯著負(fù)相關(guān)(r=-0.398、r=-0.390、r=-0.269,P值均<0.05)。胎齡、生后年齡與NAA/Cr (r=0.386、r=0.328,P值均<0.05),NAA/Cho (r=0.432、r=0.367,P值均<0.05)呈正相關(guān),與Cho/Cr (r=-0.204、r=-0.211,P值均<0.05),MI/Cr (r=-0.243、r=-0.286,P值均<0.05)呈負(fù)相關(guān)。此外,隨著DEHSI的程度增加,NAA濃度,NAA/Cr和NAA/Cho比值下降(r=-0.320、r=-0.394、r=-0.565,P值均<0.05),而Cho/Cr和MI/Cr增加(r=0.389、r=0.376,P值均<0.05)。單因素方差分析:與正常組相比,輕度DEHSI組及中重度DEHSI組Cho/Cr和MI/Cr比值顯著升高(P值均<0.05),而NAA/Cr、NAA/Cho比值顯著下降(P值均<0.05)。結(jié)論 生后年齡、胎齡、頭圍與DEHSI評(píng)估之間呈負(fù)相關(guān);胎齡及生后年齡與新生兒腦組織代謝物水平有關(guān);胎齡越大,胎兒越成熟,DEHSI分級(jí)越低,NAA濃度升高。
新生兒;腦;彌漫性高信號(hào);磁共振波譜學(xué)
彌漫性高信號(hào)(diffuse excessive high signal intensity,DEHSI)是在T2WI以正常無髓鞘化白質(zhì)為參考,在雙側(cè)腦室周圍及皮層下白質(zhì)表現(xiàn)為信號(hào)增高的一種現(xiàn)象[1]。研究表明,DEHSI可能導(dǎo)致患兒認(rèn)知、感覺神經(jīng)及行為發(fā)育障礙等[2]。磁共振波譜(MRS)可無創(chuàng)性定量檢測(cè)人體細(xì)胞生物化學(xué)和代謝變化。筆者應(yīng)用單體素1H-MRS技術(shù)對(duì)95名新生兒腦白質(zhì)進(jìn)行研究,提高對(duì)其演變發(fā)展規(guī)律的理解,明確異常代謝的病理狀態(tài),為DEHSI的早期診斷提供依據(jù)。
1.1臨床資料
選取2013年1月至2014年6月寧夏醫(yī)科大學(xué)總醫(yī)院新生兒科的95名新生兒作為研究對(duì)象,其中包括40名適于胎齡早產(chǎn)兒和55名正常足月兒。所有新生兒均無神經(jīng)功能障礙和窒息史;經(jīng)臨床、實(shí)驗(yàn)室及影像學(xué)相關(guān)檢查,存在DEHSI并排除先天代謝性疾病、先天性畸形、顱內(nèi)感染及其他腦損傷等疾病[3]。本研究經(jīng)醫(yī)院倫理委員會(huì)批準(zhǔn),檢查前均取得受試者家屬同意,并與之簽訂知情同意書。
1.2檢查方法
采用GE SignaTwin Speed 1.5T MR掃描儀,在研究對(duì)象熟睡時(shí)掃描,不能入睡者給予5%水合氯醛50 mg/kg口服鎮(zhèn)靜。檢查需在1名護(hù)士或醫(yī)師陪同下進(jìn)行,并注意患兒的保暖、聽力保護(hù)及生命體征的觀察。所有研究對(duì)象均接受常規(guī)MRI檢查(掃描參數(shù):T1 FLAIR:TR 1784 ms,TE 21.5 ms,矩陣 288×192;T2WI:TR 5400 ms,TE 111.1 ms,矩陣 320×224;T2FLAIR:TR 7800 ms,TE 146.5 ms,矩陣 320×224;所有序列層厚5 mm,層間距0.5 mm,F(xiàn)OV 24 cm×18 cm)。1H-MRS采用點(diǎn)分辨波譜(point resolved spectroscopy,PRESS)序列,自動(dòng)預(yù)掃描完成勻場(chǎng)及水抑制,興趣區(qū)置于右額葉白質(zhì)(T2WI橫軸面基底節(jié)水平),TR 1000 ms,TE 35 ms,矩陣16×8,F(xiàn)OV 11 cm×11 cm,半高帶寬<10,自動(dòng)勻場(chǎng)水抑制>98%,興趣區(qū)大?。?8 mm×18 mm×18 mm~20 mm×20 mm× 20 mm,掃描時(shí)間約3 min。以Cr作為內(nèi)參照物,采用FunctoolⅡ?qū)Σ杉腗RS數(shù)據(jù)進(jìn)行處理,分別測(cè)量N-乙酰天冬氨酸(NAA)、肌酸(Cr)、膽堿復(fù)合物(Cho)和肌醇(MI)代謝物的峰下面積,并計(jì)算不同物質(zhì)之間(NAA/Cr、NAA/Cho、Cho/Cr和MI/Cr)的比值,掃描時(shí)避開周圍顱骨,脂肪和腦脊液的影響。額葉每個(gè)興趣區(qū)T2信號(hào)值分別測(cè)量3次取其平均值,興趣區(qū)面積約30 mm2。
1.3磁共振成像分組
MR圖像分別由2名高年資放射科醫(yī)師獨(dú)立閱片評(píng)價(jià),2名醫(yī)師獨(dú)立閱片評(píng)分一致性評(píng)估采用Kappa檢驗(yàn),Kappa值=0.812,P<0.01 。根據(jù)影像學(xué)表現(xiàn)將DEHSI定性分組如下:正常:腦白質(zhì)區(qū)無高信號(hào);輕度:腦室前后角旁稍高信號(hào);中度:腦室前后角旁無邊界的彌漫性高信號(hào);重度:所有白質(zhì)區(qū)彌漫性高信號(hào)[4-5]。由于重度病例相對(duì)較少,將中重度合并為一組,結(jié)合文獻(xiàn)[6]將DEHSI分為3組:無DEHSI,輕度DEHSI,中重度DEHSI;分別測(cè)量不同分組額葉T2信號(hào)值。
1.4統(tǒng)計(jì)學(xué)方法
采用SPSS 20.0軟件包對(duì)所得數(shù)據(jù)進(jìn)行統(tǒng)計(jì)分析,計(jì)量資料以±s表示,本組資料中DEHSI與臨床指標(biāo)、代謝物比值的相關(guān)性采用Spearman相關(guān)分析。對(duì)正常組與輕度、中重度DEHSI的代謝物比值采用單因素方差分析,以P<0.05為差異具有統(tǒng)計(jì)學(xué)意義。
2.1DEHSI的分組
對(duì)無DEHSI、輕度DEHSI、中重度DEHSI(圖1)各組分別進(jìn)行定量評(píng)估,其信號(hào)值分別為1274.53±266.80、1490.32±200.90和1531.18 ±262.42(表1)。95名受試者中正常無DEHSI者25名,輕度DEHSI 者31名,中重度DEHSI者39名。
2.2圍產(chǎn)期臨床特點(diǎn)與DEHSI的關(guān)系
95名受試者平均胎齡(37.4±2.6)周;MRI掃描時(shí)平均生后年齡(13.15±7.47) d;平均體重(2866.8±675.2) g;平均頭圍(33.2±2.6) cm(表1)。胎齡、體重和頭圍兩兩之間呈正相關(guān)(胎齡與體重,胎齡與頭圍,體重與頭圍:r值分別為0.690、0.659、0.844,P均<0.05)。生后年齡、胎齡、頭圍均與DEHSI程度呈負(fù)相關(guān)(r值分別為-0.398、-0.390、-0.269,P均<0.05)。DEHSI程度與T2信號(hào)值之間呈正相關(guān)(r=0.379,P<0.05)。生后年齡與T2信號(hào)值呈負(fù)相關(guān)(r=-0.284,P<0.05)(表2)。
表1 不同信號(hào)組間的一般情況(± s)Tab. 1 Each grade of DEHSI in Infant ofThe characteristics (± s)
表1 不同信號(hào)組間的一般情況(± s)Tab. 1 Each grade of DEHSI in Infant ofThe characteristics (± s)
Group Without DEHSI (n=25)mild DEHSI (n=31)moderate-severe DEHSI (n =39) Total (n=95) Signal values 1274.53±266.80 1490.32±200.90 1531.18±262.42 1450.31±265.24 Postnatal age (days) 24.00±14.78 9.94±8.07 8.74±5.54 13.15±7.47 Gestational age (weeks) 38.46±2.04 37.87±2.09 36.30±2.90 37.38±2.59 Weight (g) 2926.00±516.89 3022.42±607.94 2705.21±786.31 2866.82±675.18 Head girth (cm) 33.82±2.34 33.68±2.19 32.41±2.80 33.19±2.56
表2 患兒DEHSI與其臨床特點(diǎn)的相關(guān)性Tab. 2 The correlation between DEHSI and clinical index
2.2圍產(chǎn)期臨床特點(diǎn)、DEHSI與MRS的關(guān)系
早產(chǎn)兒與足月兒腦內(nèi)代謝物種類相似,1H-MRS均可觀察到NAA峰、Cho峰及Cr峰 (圖2)。右額葉代謝物相對(duì)濃度比值以±s表示(表3)。NAA濃度在圍產(chǎn)期逐漸升高并與胎齡及生后天數(shù)呈正相關(guān)(r值分別為0.301、0.216,P值均<0.05)。胎齡、生后年齡與NAA/Cr (r值分別為0.386、0.328,P值均<0.05)及NAA/Cho (r值分別為0.432、0.367,P值均<0.05)呈正相關(guān);與Cho/Cr(r值分別為-0.204、-0.211,P值均<0.05)及MI/Cr (r值分別為-0.243、-0.286,P值均<0.05)呈負(fù)相關(guān)(表4)。
表3 不同信號(hào)組間代謝物的一般情況(± s)Tab. 3 Infant characteristics in each grade of DEHSI (± s)
表3 不同信號(hào)組間代謝物的一般情況(± s)Tab. 3 Infant characteristics in each grade of DEHSI (± s)
Group without DEHSI (n=25) mild DEHSI (n=31) Moderatesevere DEHSI (n=39)Total (n=95) NAA 33.24±20.22 22.65±11.65 18.21±12.11 23.61±15.63 NAA/Cr 1.36±0.23 1.15±0.21 1.11±0.19 1.19±0.23 Cho/Cr 1.38±0.21 1.53±0.31 1.63±0.24 1.53±0.27 Ml/Cr 1.10±0.31 1.37±0.29 1.48±0.36 1.34±0.36 NAA/Cho 1.10±0.21 0.77±0.16 0.69±0.14 0.79±0.21
表4 胎齡、生后天數(shù)和DEHSI與各代謝物比值的相關(guān)性分析Tab. 4 The relationship between MRS ratios and GA、Postnatal age and DEHSI
隨著新生兒腦白質(zhì)DEHSI程度的增加,NAA濃度、NAA/Cr 和 NAA/Cho比值顯著下降 (r值分別為-0.320、-0.394、-0.565,P值均<0.05),Cho/Cr和 MI/Cr比值上升(r值分別為0.389、0.376,P值均<0.05)(表4)。采用單因素方差分析分別對(duì)患兒正常組與輕度、中重度DEHSI的代謝物比值進(jìn)行評(píng)估,正常組和輕度、正常組與中重度DEHSI的代謝物比值相比較,NAA/Cr、NAA/Cho、Cho/Cr和MI/Cr四項(xiàng)指標(biāo)均具有統(tǒng)計(jì)學(xué)意義(P值均<0.05;表5)。
圖1 T2WI上DEHSI分度圖。A:男,7 d,36+5周,腦白質(zhì)區(qū)無高信號(hào);B:男,3 d,35+4周,腦室前后角旁稍高信號(hào),可見邊界(箭頭);C:男,7 d,35+2周,所示白質(zhì)區(qū)均呈彌漫性高信號(hào),腦室前后角旁無邊界。右額葉ROI面積均為(30±1) mm2圖2 A,B:正常足月兒右額葉波譜圖,男,年齡5 d,胎齡37+5周,NAA/Cr=1.07。C,D:早產(chǎn)兒DEHSI右額葉波譜圖,男,年齡4 d,胎齡36+5周,NAA/Cr=1.03Fig. 1 Samples of different grades of DEHSI are viewed onT2WI. A: Male, 7 days, 36+5weeks, no DEHSIThroughoutThe white matter. B: Male, 3 days, 35+4weeks, high signal intensity is visible only withinThe crossroads (arrow). C: Male, 7 days, 35+2weeks, widespread high signal intensity is visible inThe entire cerebral white matter.The ROI ofThe signal value is measured inThe right frontal area,The area is about (30±1) mm2. Fig. 2 A, B:The MRS inThe right frontal white matter of normalTerm infant, male, 5 days, 37+5weeks, NAA/Cr=1.07. C, D:The MRS inThe right frontal white matter of preterm with DEHSI, male, 4 days, 36+5weeks, NAA/Cr=1.03.
表5 DEHSI 3組間代謝物比值的單因素方差分析Tab. 5 One-way ANOVA was performedThoughThree DEHSI groups’ ratios
胎兒在母體處于動(dòng)態(tài)發(fā)育過程,胎兒的體重、頭圍等呈上升曲線,目前衡量新生兒生長(zhǎng)發(fā)育的標(biāo)志很多,如體重、頭圍等。本組數(shù)據(jù)證實(shí),隨著胎齡的增加,體重與頭圍呈增長(zhǎng)趨勢(shì)。此外,胎兒出生以后宮外環(huán)境暴露時(shí)間增加是DEHSI程度減低的相關(guān)因素,從而促進(jìn)嬰兒成熟度增高[7]。DEHSI可見于胎兒和新生兒時(shí)期,隨后消失,因此在嬰兒腦發(fā)育過程中呈動(dòng)態(tài)變化[8]。
NAA 位于2.02 ppm,存在于少突膠質(zhì)前體細(xì)胞,是軸突病變標(biāo)記物。Cho 位于3.20 ppm,是新生兒腦組織MRS最高峰,隨著腦發(fā)育髓鞘化其濃度降低。Cr 位于3.02 ppm,是神經(jīng)胞質(zhì)內(nèi)的高能磷酸儲(chǔ)備,Cr總量在腦內(nèi)不同代謝條件下相對(duì)比較穩(wěn)定,因此在本研究作為內(nèi)標(biāo)準(zhǔn)。MI位于3.56 ppm,代表腦成熟,是直接參與神經(jīng)信號(hào)系統(tǒng)的一個(gè)重要指標(biāo)。本研究結(jié)果表明在腦發(fā)育過程中NAA濃度逐漸上升而Cho與Ml濃度逐漸下降,與文獻(xiàn)[6,9]研究結(jié)果一致。
NAA是在神經(jīng)元/神經(jīng)軸突線粒體合成,沿著軸突向下擴(kuò)散,并為髓鞘脂質(zhì)合成提供乙?;诔墒焐偻荒z質(zhì)細(xì)胞內(nèi)降解,因此,NAA在細(xì)胞水平降解,組織損傷將導(dǎo)致軸突成熟延遲,此外,未成熟的少突膠質(zhì)細(xì)胞也可合成NAA[10]。NAA是大腦發(fā)育過程中,腦成熟和髓鞘化的指標(biāo)之一。在髓鞘化階段,未成熟少突膠質(zhì)細(xì)胞開始進(jìn)入軸突,轉(zhuǎn)化為少突膠質(zhì)細(xì)胞祖細(xì)胞[11]。但是,未成熟少突膠質(zhì)細(xì)胞可能不會(huì)成為髓鞘成熟生成細(xì)胞。少突膠質(zhì)細(xì)胞的演變導(dǎo)致軸索大小、軸突細(xì)胞膜和胞內(nèi)成分的變化,從而影響腦白質(zhì)的細(xì)胞外間隙和含水量下降[12]。膜密度改變依賴于未成熟少突膠質(zhì)細(xì)胞破壞,進(jìn)而導(dǎo)致未成熟少突膠質(zhì)細(xì)胞進(jìn)入軸突故障。因此,延遲成熟或組織損傷時(shí)軸突和細(xì)胞外水分子的變化可能是T2WI信號(hào)變化的原因[10]。早產(chǎn)兒腦白質(zhì)損傷主要表現(xiàn)為髓鞘化過程中50%~90%少突神經(jīng)膠質(zhì)和軸突及膠質(zhì)細(xì)胞成分的枯竭[13]。文獻(xiàn)報(bào)道,DEHSI可能代表少突膠質(zhì)細(xì)胞和(或)軸突異常[14]。DEHSI中NAA的降低與未成熟少突膠質(zhì)細(xì)胞損傷及其演變過程中進(jìn)入軸突障礙有關(guān)[15]。本組腦白質(zhì)DEHSI隨程度的增加,NAA濃度、NAA/Cr 和 NAA/Cho比值顯著下降,呈負(fù)相關(guān)也證實(shí)了這一結(jié)論。
近年來,隨著新生兒監(jiān)護(hù)水平不斷提高及疾病診治策略日益完善,新生兒死亡率已明顯降低,但新生兒腦損傷致殘仍普遍存在。DEHSI是國(guó)外醫(yī)學(xué)界研究的熱點(diǎn),國(guó)內(nèi)鮮有報(bào)道。Counsell 等[16]認(rèn)為嬰兒腦白質(zhì)DEHSI是成熟延遲的表現(xiàn),而非永久性白質(zhì)損傷。未成熟少突膠質(zhì)細(xì)胞在預(yù)產(chǎn)期前最后3個(gè)月極其脆弱[17],因此這一時(shí)期未成熟少突膠質(zhì)細(xì)胞受損是最常見的早產(chǎn)兒腦損傷形式[18]。有學(xué)者認(rèn)為DEHSI中NAA/Cr的降低與早產(chǎn)兒腦白質(zhì)損傷有關(guān),DEHSI可能提示認(rèn)知發(fā)育不良[2]。Dyet等[19]通過119例早產(chǎn)兒磁共振成像研究證實(shí)DEHSI與神經(jīng)發(fā)育不良有顯著相關(guān)性,認(rèn)為腦白質(zhì)DEHSI可預(yù)測(cè)矯正年齡后18~36個(gè)月的輕度發(fā)育延遲,中重度DEHSI會(huì)有較差的認(rèn)知發(fā)展。DEHSI的細(xì)胞學(xué)及解剖學(xué)基礎(chǔ)尚存爭(zhēng)議,因此DEHSI能否代表輕度腦白質(zhì)損傷或成熟延遲有待進(jìn)一步證實(shí)[10]。
本研究的局限性:(1)T2WI信號(hào)可能受到的磁場(chǎng)非均勻性影響,磁場(chǎng)不均勻性與DEHSI信號(hào)強(qiáng)度混淆。(2)單體素技術(shù)在腦組織覆蓋范圍及空間分辨率方面較局限。(3) DEHSI是指矯齡后的早產(chǎn)兒,本組部分病例尚未達(dá)到矯齡,可能會(huì)造成數(shù)據(jù)偏倚。 近些年MRS極大地拓展和豐富了磁共振成像在新生兒腦組織發(fā)育功能和腦損傷評(píng)價(jià)的應(yīng)用價(jià)值。DEHSI逐漸受到了新生兒領(lǐng)域的關(guān)注,因此,準(zhǔn)確地揭示DEHSI嚴(yán)重程度的形式和量化標(biāo)準(zhǔn),識(shí)別潛在高危早產(chǎn)兒并行神經(jīng)保護(hù)和早期干預(yù)治療是預(yù)后的關(guān)鍵。
[
[1] Plaisier A, Govaert P, Lequin MH, et al. OptimalTiming of cerebral MRI in preterm infantsTo predict long-term neurodevelopmental outcome: a systematic review. AJNR Am J Neuroradiol, 2014, 35(5): 841-847.
[2] Kidokoro H, Anderson PJ, Doyle LW, et al. High signal intensity onT2-weighted MR imaging atTerm-equivalent age in preterm infants does not predict 2-year neurodevelopmental outcomes. AJNR Am J Neuroradiol, 2011, 32(11): 2005-2010.
[3] Liu LL, Bo RT, Yang WJ, et al. DiffusionTensor imaging study of normal neonatal brain maturation. Chin J Magn Reson Imaging, 2015, 6(4): 253-257.
劉嶺嶺, 孛茹婷, 楊文君, 等. 磁共振彌散張量成像技術(shù)在新生兒腦白質(zhì)發(fā)育中的研究. 磁共振成像, 2015, 6(4): 253-257.
[4] Weinstein M, Bashat DB, Gross-Tsur V, et al. Isolated mild white matter signal changes in preterm infants: a regional approach for comparison of cranial ultrasound and MRI findings. J Perinatol, 2014, 34(6): 476-482.
[5] Bhakoo KK, Williams IT, Williams SR, et al. Proton nuclear magnetic resonance spectroscopy of primary cells derived from nervousTissue. J Neurochem, 1996, 66(3): 1254-1263.
[6] Jessica L, Wisnowsk I, Vincent J, et al. Magnetic resonance spectroscopy markers of axons and astrogliosis in relationTo specific features of white matter injury in preterm infants. Neuroradiology, 2014, 56(9): 771-779.
[7] Groppo M, Ricci D, Bassi L, et al. Development ofThe optic radiations and visual function after premature birth. Cortex, 2014, 56: 30-37.
[8]TaokaT, Aida N, OchiT, et al.Transient hyperintensity inThe subthalamic nucleus and globus pallidus of newborns onT1-weighted images. AJNR Am J Neuroradiol, 2011, 32(6): 1130-1137.
[9] Ye BB.The value of magnetic resonance imaging in children with nervous system.Nanjimg:The 14th National Conference on Radiology, 2007: 193-194.
葉濱賓. 磁共振成像在小兒神經(jīng)系統(tǒng)中的應(yīng)用價(jià)值. 南京: 第十四次全國(guó)放射學(xué)學(xué)術(shù)會(huì)議, 2007: 193-194.
[10] Hagmann CF, De Vita E, Bainbridge A, et al.T2 at MR imaging is an objective quantitative measure of cerebral white matter signal intensity abnormality in preterm infants atTerm-equivalent age 1. Radiology, 2009, 252(1): 209-217.
[11] Sizonenko SV, Camm EJ, Dayer A, et al. Glial responsesTo neonatal hypoxicischemic injury inThe rat cerebral cortex. Int J Dev Neurosci, 2008, 26(1): 37-45.
[12] Miller S, Vigneron D, Henry R, et al. Serial quantitative diffusion
tensorMRIofThe premature brain: development in newborns with andwithout injury. J Magn Reson Imaging, 2002, 16(6): 621-632.
[13] Back SA, Riddle A, McClure MM. Maturation-dependent vulnerability of perinatal white matter in premature birth. Stroke, 2007, 38(2 Suppl): 724-730.
[14] Ski?ld B, Horsch S, Hallberg B, et al. White matter changes in extremely preterm infants, a population-based diffusionTensor imaging study. Acta Paediatr, 2010, 99(6): 842-849.
[15] Volpe JJ. Neurology ofThe newborn. 5th ed. Philadelphia: Saunders, 2008: 414-427.
[16] Counsell SJ, Shen Y, Boardman JP, et al. Axial and radial diffusivity in preterm infants who have diffuse white matter changes on magnetic resonance imaging atTerm-equivalent age. Pediatrics, 2006, 117(2): 376-386.
[17] Haynes RL, Folkerth RD, Keefe RJ, et al. Nitrosative and oxidative injuryTo premyelinating oligodendrocytes in periventricular leukomalacia. J Neuropathol Exp Neurol, 2003, 62(5): 441-450.
[18] Volpe JJ. Brain injury in premature infants: a complex amalgam of destructive and developmental disturbances. Lancet Neurol, 2009, 8(1): 110-124.
[19] Dyet LE, Kennea N, Counsell SJ, et al. Natural history of brain lesions in extremely preterm infants studied with serial magnetic resonance imaging from birth and neurodevelopmental assessment. Pediatrics, 2006, 118(8): 536-548.
Applications of1H-MRS and clinical relative factors in diagnosis of neonatal cerebral white matter diffuse excessive high signal intensity
BO Ru-ting1, Ji Guang-hai1, Zheng Yi1, LIU Ling-ling2, WU Yu-hua3, YANG Wen-jun4, CHEN Zhi-qiang2*
1Ningxia Medical University , Yinchuan 750004, China
2Department of Radiology, General Hospital of Ningxia Medical University, Yinchuan 750004, China
3Department of Neonatology, General Hospital of Ningxia Medical University, Yinchuan 750004, China
4Key Laboratory of Fertility Maintenance, Ministry of Education, Ningxia Medical University, Yinchuan 750004, China
*CorrespondenceTo: Chen ZQ, E-mail: zhiqiang_chen99@163.com
19 Aug 2015, Accepted 5 Oct 2015
Objective: Use proton magnetic resonance spectroscopy (1H-MRS)To observeThe imaging features in neonatal cerebral white matter diffuse excessive high signal (DEHSI) and exploreThe evolution of DEHSI and diagnostic value. Materials and Methods:This study included 95 neonates, using MRS forThe study ofThe region of interest in cerebral white matter lesions. Results: Postnatal age, gestational age, and head girth had significantly negative correlation with DEHSI (r=-0.398, r= -0.390, r=-0.269, all P<0.05). Gestational age and postnatal age withThe ratios of NAA/Cr (r=0.386, r=0.328, all P<0.05), and NAA/Cho (r=0.432, r=0.367, all P<0.05) were discovered with a clearly positive signifcant difference and a marked negatively correlated withThe values Cho/Cr (r=-0.204, r=-0.211, all P<0.05), and MI/Cr(r=-0.243, r=-0.286, all P<0.05). In addition,The increasing extent of DEHSI was associated with a signifcant decrease in NAA concentration, NAA/Cr in relationTo NAA/Cho (r=-0.320, r=-0.394, r=-0.565, all P<0.05), resulting in an increase in Cho/Cr and MI/Cr (r=0.389, r=0.376, all P<0.05). Compared with control group, Cho/Cr and MI/Cr were signifcantly elevated, whereas NAA/Cr and NAA/Cho ratios were signifcantly decreased in infants with mild DEHSI and moderate-sereve DEHSI (all P<0.05). Conclusions: Postnatal age, gestational age, and head girth had negative correlation with DEHSI. Gestational age and postnatal age were relatedTo metabolite levels in neonatal brain. In addition, when it stayed in intrauterine forThe longTime, and it hadThe higher maturity,The lower grade of DEHSI, which was resulting in elevating NAA concentrations.
Neonate; Brain; Diffuse excessive high signal intensity; Magnetic resonance spectroscopy
寧夏科技攻關(guān)項(xiàng)目資助(編號(hào):W2015);銀川市科技攻關(guān)資助項(xiàng)目(編號(hào):W2015-4);寧夏醫(yī)科大學(xué)重點(diǎn)項(xiàng)目(編號(hào):XM2014)
作者單位:
1.寧夏醫(yī)科大學(xué),銀川 750004
2.寧夏醫(yī)科大學(xué)總醫(yī)院放射科,銀川750004
3.寧夏醫(yī)科大學(xué)總醫(yī)院新生兒科,銀川 750004
4.寧夏醫(yī)科大學(xué)生育力保持教育部重點(diǎn)實(shí)驗(yàn)室,銀川 750004
陳志強(qiáng),E-mail:zhiqiang_chen99 @163.com
R445.2;R742
A
10.3969/j.issn.1674-8034.2015.11.003
孛茹婷, 姬廣海, 鄭義, 等.1H-MRS和臨床相關(guān)因素在新生兒腦白質(zhì)彌漫性高信號(hào)診斷中的應(yīng)用價(jià)值. 磁共振成像, 2015, 6(11): 812-817.
ACKNOWLEDGMENTSThis work was part ofThe Program of Science andTechnology Foundation of Ningxia (No. W2015).The work was supported by Yinchuan Science andTechnology Key Projects Fund (No. W2015-4).The work was supported by Key Project of Ningxia Medical University (No. XM2014).