动态观察新生儿缺氧缺血性脑病的CT改变
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摘要
目的：通过对我院儿科2003年3月至2004年12月收治的75例怀疑新生儿缺氧缺血性脑病(Neonatal Hypoxic-ischemic Encephalopathy HIE)的新生儿的CT表现及临床表现进行比较分析,研究新生儿缺氧缺血性脑病的CT表现,分析新生儿缺氧缺血性脑病的CT分级与临床分级的关系,研究新生儿缺氧缺血性脑病伴发颅内出血的CT表现,分析新生儿缺氧缺血性脑病的分级与颅内出血的关系,分析颅内出血的CT诊断和临床诊断的关系,将随诊CT表现进行分析,评估预后情况。
方法：75例怀疑新生儿缺氧缺血性脑病患儿用10%的水合氯醛按照0.5ml/kg的剂量保留灌肠后,进行CT检查,分析新生儿缺氧缺血性脑病及其并发的颅内出血的CT表现及其特点,并将CT分级与临床分级比较,分析两者之间的关系。将临床颅内出血的诊断与CT诊断进行比较,判断两者之间是否存在差异。比较新生儿缺氧缺血性脑病的CT分级与其伴发颅内出血之间的关系。分别在一个半月、三个月、六个月、一年共对48例患儿进行随诊观察,并对其进行CT检查,了解其治疗后脑部发育情况。
结果：缺氧缺血性脑病的病理改变主要有脑水肿,选择性神经元坏死、脑室旁白质脑软化、基底节区大理石样变、矢状旁区脑损伤、局灶性和多发性腔隙性脑梗塞。脑水肿在CT上均表现为低密度灶,灰白质界限模糊不清,局部脑沟、脑裂变浅,双侧侧脑室缩小；脑室旁脑白质脑软化灶在CT上表现为低密度灶,边界清楚；局灶性和多发性腔隙性脑梗塞表现为斑片状低密度灶,边界不清,与脑水肿在CT上不易区分。新生儿缺氧缺血性脑病发生部位以顶叶最多见,额叶次之,枕叶再次之,颞叶最少见。新生儿缺氧缺血性脑病大多数同时伴发有颅内出血：脑实质内出血、蛛网膜下腔出血、侧脑室室管膜下出血、硬膜下血肿,其中主要为蛛网膜下腔出血,蛛网膜下腔出血几乎全部位于后颅凹(大脑大静脉池、后纵裂池、窦汇),表现为高密度影,并且向周围脑沟延伸,边界欠清,由于出血量少,没有成人蛛网膜下腔出血的高脚杯征、空心三角征,脑沟、脑裂内也没有出血征象：脑实质内出血主要为斑点状出血,CT上表现为斑点状高密度影；侧脑室室管膜下出血,CT上表现为侧脑室下条状高密度影。新生儿缺氧缺血性脑病伴发的颅内出血与其CT分级成正比关系。CT随诊发现有52.1%的患儿恢复正常,16.7%的患儿有侧脑室旁或顶叶白质脑软化灶,22.9%的患儿随诊CT表现有外部性脑积水,4.2%的患儿有外部性脑积水同时伴有侧脑室旁白质脑软化灶。将新生儿缺氧缺血性脑病患儿的CT分级和临床分级进行比较,存在明显差异。新生儿缺氧缺血性脑病合并颅内出血的CT诊断和临床诊断存在明显差异。新生儿缺氧缺血性脑病合并颅内出血和CT分级存在明显关系,轻度新生儿缺氧缺血性脑病患儿61.5%合并颅内出血,中度新生儿缺氧缺血性脑病患儿69.7%合并颅内出血,重度新生儿缺氧缺血性脑病患儿100%合并颅内出血。
结论：新生儿缺氧缺血性脑病临床表现和CT表现不一致,新生儿缺氧缺血性脑病合并颅内出血CT诊断和临床诊断存在明显差异,因此新生儿缺氧缺血性脑病的正确诊断,需要临床和CT相结合。正常新生儿的额叶CT上也可以表现为低密度灶,新生儿缺氧缺血性脑病CT上的低密度灶应与正常的新生儿额叶低密度区相鉴别,对称性、灰白质分界清楚是正常发育新生儿的额叶低密度区的主要特点。新生儿缺氧缺血性脑病大多数同时伴发颅内出血,主要为蛛网膜下腔出血,主要位于后颅凹(大脑大静脉池、后纵裂池、窦汇),这些部位应该是阅片时重点观察的部位。新生儿缺氧缺血性脑病合并颅内出血与CT分级有明显关系,缺氧缺血程度越重合并颅内出血的几率越大。CT随诊可以观察治疗后的脑实质发育情况,并且通过治疗前后对比,了解病变的变化。
Objective:CT manifestations and clinical performance of 75 newborns who were suspected of neonatal hypoxic-ischemic encephalopathy (Neonatal Hypoxic-ischemic Encephalopathy HIE) were analyzed and compared, the following questions were addressed,1) CT manifestations of HIE encephalopathy,2) Relationship between neonatal HIE CT grading and clinical classification,3) If the intracranial hemorrhage's CT manifestations associated with neonatal HIE,4) Relationship between the classification of neonatal HIE and intracranial hemorrhage,5) Relationship between the CT diagnosis of intracranial hemorrhage and clinical diagnosis,6) Association between the following up CT manifestations and the prognosis of the patients.
Methods:10%of the chloral hydrate in dose of 0.5ml/kg was conducted to 75 newborns with suspected HIE by ways of retention enema before the CT examination. Manifestations and characteristics of neonatal HIE with concurrent intracranial hemorrhage in CT examination were observed. Then the CT grading and clinical classification were campared and analyzed, the accordance of clinical diagnosis of intracranial hemorrhage and CT results were accessed, and the relationship between the CT grading of neonatal HIE and rate of intracranial hemorrhage were studied. To understand the brain restoration and deveplopment after treatment,48 cases were followed up for observation, at one and a half months, three months, six months, one year, their CT results were accessed.
Results:The main pathological changes of HIE include cerebral edema, selective neuronal necrosis, periventricular white matter encephalomalacia, basal ganglia marble-like change, brain damage adjacent to sagittal area, focal and multiple lacunar cerebral infarctions. Cerebral edema on the CT showed low density, boundaries of gray and white matter blurred, regional cerebral sulcus and fission shallowed, bilateral lateral ventricle narrowed. Periventricular white matter encephalomalacia showed low density lesions on CT, the border was clear. Focal and multiple lacunar infarction showed patchy low-density lesion, the border was unclear, which was difficult differentiated from brain edema on CT. The most common location of neonatal HIE was parietal lobe, followed by frontal lobe, occipital lobe, the temporal lobe was rare. Majority of neonatal HIE are associated with intracranial hemorrhage: hemorrhage in cerebral parenchyma, subarachnoid hemorrhage, subendymal hemorrhage in lateral ventricle, mainly as a subarachnoid hemorrhage, almost all in the posterior fossa (cerebral vein pool, posterior longitudinal crack pool, sinus exchange), manifesting as high-density shadow, which extending to the periphery of sulcus and the border was blur. Due to less bleeding, there was no subarachnoid hemorrhage goblet sign, hollow triangle sign and also no sign of bleeding in cerebral sulcus and fissure which was common in adults. Most of the intracranial hemorrhage was patchy hemorrhage, whic demonstrated as patchy high density shadow on CT. Lateral ventricle subependymal hemorrhage displayed as high-density shadow in the lateral ventricle on CT. CT classification of neonatal HIE was positive related to the rate of intracranial hemorrhage. The CT following up showed that 52.1% of the children returned to normal,16.7%had encephalomalacia foci of white matter in the parietal lobe adjacent to lateral ventricle,22.9%had external hydrocephalus,4.2%had external hydrocephalus accompanied by white matter encephalomalacia foci in the parietal lobe adjacent to lateral ventricle. There are significant differences between the CT grading and clinical grading of the newborns HIE. CT diagnosis disagreed with the clinical diagnosis of intracranial hemorrhage in neonatal HIE. The risk of intracranial hemorrhage in neonatal HIE was significantly related to the CT grading of neonatal HIE: 61.5%of low-grade neonatal HIE accompanied by intracranial hemorrhage, 69.7%of moderate HIE accompanied by intracranial hemorrhage,100%of severe HIE accompanied by subarachnoid hemorrhage.
Conclusion:Clinical manifestations and CT manifestations of the neonatal HIE are inconsistent. CT diagnosis and clinical diagnosis of intracranial hemorrhage associated with neonatal HIE are significant inconsistent, therefore the correct diagnosis and treatment need to combine clinical manifestations and CT results. Low-density lesions of neonatal HIE on CT should be differentiated from the normal. Sometimes CT manifestations in the frontal lobe of normal newborns showed as a low-density lesions, but the lesion was symmetry, and boundaries of gray and matter are clear. Majority of the neonatal HIE associated with intracranial hemorrhage, mainly was subarachnoid hemorrhage and mostly located in the posterior fossa (brain, large vein pool, posterior longitudinal crack pool, sinus exchange). These sites need more attention when reading films. There was significant relationship between CT grading of neonatal HIE and the rate of intracranial hemorrhage. The more severe of neonatal HIE, the greater risk of intracranial hemorrhage. CT following up can observe the condition of cerebral recovery and development after treatment. Comparing CT results before and after treatment, we can get better understanding of the pathological changes in HIE.
方法：75例怀疑新生儿缺氧缺血性脑病患儿用10%的水合氯醛按照0.5ml/kg的剂量保留灌肠后,进行CT检查,分析新生儿缺氧缺血性脑病及其并发的颅内出血的CT表现及其特点,并将CT分级与临床分级比较,分析两者之间的关系。将临床颅内出血的诊断与CT诊断进行比较,判断两者之间是否存在差异。比较新生儿缺氧缺血性脑病的CT分级与其伴发颅内出血之间的关系。分别在一个半月、三个月、六个月、一年共对48例患儿进行随诊观察,并对其进行CT检查,了解其治疗后脑部发育情况。
结果：缺氧缺血性脑病的病理改变主要有脑水肿,选择性神经元坏死、脑室旁白质脑软化、基底节区大理石样变、矢状旁区脑损伤、局灶性和多发性腔隙性脑梗塞。脑水肿在CT上均表现为低密度灶,灰白质界限模糊不清,局部脑沟、脑裂变浅,双侧侧脑室缩小；脑室旁脑白质脑软化灶在CT上表现为低密度灶,边界清楚；局灶性和多发性腔隙性脑梗塞表现为斑片状低密度灶,边界不清,与脑水肿在CT上不易区分。新生儿缺氧缺血性脑病发生部位以顶叶最多见,额叶次之,枕叶再次之,颞叶最少见。新生儿缺氧缺血性脑病大多数同时伴发有颅内出血：脑实质内出血、蛛网膜下腔出血、侧脑室室管膜下出血、硬膜下血肿,其中主要为蛛网膜下腔出血,蛛网膜下腔出血几乎全部位于后颅凹(大脑大静脉池、后纵裂池、窦汇),表现为高密度影,并且向周围脑沟延伸,边界欠清,由于出血量少,没有成人蛛网膜下腔出血的高脚杯征、空心三角征,脑沟、脑裂内也没有出血征象：脑实质内出血主要为斑点状出血,CT上表现为斑点状高密度影；侧脑室室管膜下出血,CT上表现为侧脑室下条状高密度影。新生儿缺氧缺血性脑病伴发的颅内出血与其CT分级成正比关系。CT随诊发现有52.1%的患儿恢复正常,16.7%的患儿有侧脑室旁或顶叶白质脑软化灶,22.9%的患儿随诊CT表现有外部性脑积水,4.2%的患儿有外部性脑积水同时伴有侧脑室旁白质脑软化灶。将新生儿缺氧缺血性脑病患儿的CT分级和临床分级进行比较,存在明显差异。新生儿缺氧缺血性脑病合并颅内出血的CT诊断和临床诊断存在明显差异。新生儿缺氧缺血性脑病合并颅内出血和CT分级存在明显关系,轻度新生儿缺氧缺血性脑病患儿61.5%合并颅内出血,中度新生儿缺氧缺血性脑病患儿69.7%合并颅内出血,重度新生儿缺氧缺血性脑病患儿100%合并颅内出血。
结论：新生儿缺氧缺血性脑病临床表现和CT表现不一致,新生儿缺氧缺血性脑病合并颅内出血CT诊断和临床诊断存在明显差异,因此新生儿缺氧缺血性脑病的正确诊断,需要临床和CT相结合。正常新生儿的额叶CT上也可以表现为低密度灶,新生儿缺氧缺血性脑病CT上的低密度灶应与正常的新生儿额叶低密度区相鉴别,对称性、灰白质分界清楚是正常发育新生儿的额叶低密度区的主要特点。新生儿缺氧缺血性脑病大多数同时伴发颅内出血,主要为蛛网膜下腔出血,主要位于后颅凹(大脑大静脉池、后纵裂池、窦汇),这些部位应该是阅片时重点观察的部位。新生儿缺氧缺血性脑病合并颅内出血与CT分级有明显关系,缺氧缺血程度越重合并颅内出血的几率越大。CT随诊可以观察治疗后的脑实质发育情况,并且通过治疗前后对比,了解病变的变化。
Objective:CT manifestations and clinical performance of 75 newborns who were suspected of neonatal hypoxic-ischemic encephalopathy (Neonatal Hypoxic-ischemic Encephalopathy HIE) were analyzed and compared, the following questions were addressed,1) CT manifestations of HIE encephalopathy,2) Relationship between neonatal HIE CT grading and clinical classification,3) If the intracranial hemorrhage's CT manifestations associated with neonatal HIE,4) Relationship between the classification of neonatal HIE and intracranial hemorrhage,5) Relationship between the CT diagnosis of intracranial hemorrhage and clinical diagnosis,6) Association between the following up CT manifestations and the prognosis of the patients.
Methods:10%of the chloral hydrate in dose of 0.5ml/kg was conducted to 75 newborns with suspected HIE by ways of retention enema before the CT examination. Manifestations and characteristics of neonatal HIE with concurrent intracranial hemorrhage in CT examination were observed. Then the CT grading and clinical classification were campared and analyzed, the accordance of clinical diagnosis of intracranial hemorrhage and CT results were accessed, and the relationship between the CT grading of neonatal HIE and rate of intracranial hemorrhage were studied. To understand the brain restoration and deveplopment after treatment,48 cases were followed up for observation, at one and a half months, three months, six months, one year, their CT results were accessed.
Results:The main pathological changes of HIE include cerebral edema, selective neuronal necrosis, periventricular white matter encephalomalacia, basal ganglia marble-like change, brain damage adjacent to sagittal area, focal and multiple lacunar cerebral infarctions. Cerebral edema on the CT showed low density, boundaries of gray and white matter blurred, regional cerebral sulcus and fission shallowed, bilateral lateral ventricle narrowed. Periventricular white matter encephalomalacia showed low density lesions on CT, the border was clear. Focal and multiple lacunar infarction showed patchy low-density lesion, the border was unclear, which was difficult differentiated from brain edema on CT. The most common location of neonatal HIE was parietal lobe, followed by frontal lobe, occipital lobe, the temporal lobe was rare. Majority of neonatal HIE are associated with intracranial hemorrhage: hemorrhage in cerebral parenchyma, subarachnoid hemorrhage, subendymal hemorrhage in lateral ventricle, mainly as a subarachnoid hemorrhage, almost all in the posterior fossa (cerebral vein pool, posterior longitudinal crack pool, sinus exchange), manifesting as high-density shadow, which extending to the periphery of sulcus and the border was blur. Due to less bleeding, there was no subarachnoid hemorrhage goblet sign, hollow triangle sign and also no sign of bleeding in cerebral sulcus and fissure which was common in adults. Most of the intracranial hemorrhage was patchy hemorrhage, whic demonstrated as patchy high density shadow on CT. Lateral ventricle subependymal hemorrhage displayed as high-density shadow in the lateral ventricle on CT. CT classification of neonatal HIE was positive related to the rate of intracranial hemorrhage. The CT following up showed that 52.1% of the children returned to normal,16.7%had encephalomalacia foci of white matter in the parietal lobe adjacent to lateral ventricle,22.9%had external hydrocephalus,4.2%had external hydrocephalus accompanied by white matter encephalomalacia foci in the parietal lobe adjacent to lateral ventricle. There are significant differences between the CT grading and clinical grading of the newborns HIE. CT diagnosis disagreed with the clinical diagnosis of intracranial hemorrhage in neonatal HIE. The risk of intracranial hemorrhage in neonatal HIE was significantly related to the CT grading of neonatal HIE: 61.5%of low-grade neonatal HIE accompanied by intracranial hemorrhage, 69.7%of moderate HIE accompanied by intracranial hemorrhage,100%of severe HIE accompanied by subarachnoid hemorrhage.
Conclusion:Clinical manifestations and CT manifestations of the neonatal HIE are inconsistent. CT diagnosis and clinical diagnosis of intracranial hemorrhage associated with neonatal HIE are significant inconsistent, therefore the correct diagnosis and treatment need to combine clinical manifestations and CT results. Low-density lesions of neonatal HIE on CT should be differentiated from the normal. Sometimes CT manifestations in the frontal lobe of normal newborns showed as a low-density lesions, but the lesion was symmetry, and boundaries of gray and matter are clear. Majority of the neonatal HIE associated with intracranial hemorrhage, mainly was subarachnoid hemorrhage and mostly located in the posterior fossa (brain, large vein pool, posterior longitudinal crack pool, sinus exchange). These sites need more attention when reading films. There was significant relationship between CT grading of neonatal HIE and the rate of intracranial hemorrhage. The more severe of neonatal HIE, the greater risk of intracranial hemorrhage. CT following up can observe the condition of cerebral recovery and development after treatment. Comparing CT results before and after treatment, we can get better understanding of the pathological changes in HIE.
引文
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1.韩玉昆,许植之,虞人杰.新生儿缺氧缺血性脑病.1版.北京：人民卫生出版社2000年.
2.王慕狄.儿科学.五版.北京：人民卫生出版社,2001年.
3.马晓燕,刘永林.新生儿缺氧缺血性脑病63例颅脑CT诊断分析.实用医技杂志,2009年9月；16(9)：708—709.
4.李贵生.新生儿缺血缺氧性脑病的CT表现及治疗原则.实用医技杂志,2004年1月;11(1)：25.
5.张雪斌,周珉.CT在评价小儿颅内出血中的价值.实用医技杂志,2003年12月;10(12)：1353—1354.
6.刘玉花,姜山,肖格林.新生儿缺氧缺血性脑病的CT诊断.实用放射学杂志,2002年6月；18(6)：514—515.
7.金新安,蔡淑芳,姜锐松,敖振杰.早产儿与足月儿缺血缺氧性脑病的CT对照分析.实用放射学杂志,2001年6月;17(6)：462—464.
8.袁斌.新生儿缺血缺氧性脑病的CT诊断.江西医学院学报,2003；43(4)：54.
9.徐宗芳.599例患儿脑部疾病头颅CT的应用意义.临床儿科杂志,1999年;14(4)：256—257.
10.杨州,李莉媛,李健丁,张跃珍.CT检查在小儿癫痫诊断中的价值.中国医学影像技术,2003；19(2)：158—160.
11.李启桃,蔡毅勇,张家祥.64例新生儿缺血缺氧性脑病的CT诊断.上海医学影像杂志,1995;4(2)：84—86.
12.蒋敏.新生儿缺血缺氧性脑病CT应用价值.镇江医学院学报,1996,6(2)：150.
13.吕雷,米延,张丽杰,赵德超.新生儿脑疾病临床与CT诊断对照分析.哈尔滨医科大学学报,1994;28(6)：495、515.
14.陈惠金,谢丽娟,陈冠仪,朱杰明.新生儿矢状区损伤的头颅MRI和CT的诊断
特征.中华放射学杂志,2001年9月；35(9)：716—717.
15.龙晚生,罗学毛,梁长虹,李晓群.儿童脑室周围白质软化症的临床和MRI诊断.中华放射学杂志,1998年5月;32(5)：303—305.
16.虞人杰.新生儿缺氧性脑病临床及CT诊断存在的问题.中国实用儿科杂志,
2000;15：340-341.
17.韩玉昆,虞人杰,卜定方.新生儿缺氧缺血性脑病临床诊断依据和分度.中华儿科杂志,1990；28：31.
18.韩玉昆,整理.新生儿缺氧缺血性脑病诊断依据和临床分度.中华儿科杂志,1997； 35：99.
19.龚金山,刘智勇,刘宝治.新生儿缺氧缺血性脑病的CT诊断.云鹤,王立平,高宝山.内蒙古自治区医学科学论文选编.呼和浩特：远方出版社,1998.117.
20.方红.CT"反转征”—儿童缺氧／缺血性脑损伤的结果.国外医学：临床放射学分册,1990：13：349.
21.方国涛,周世铮,周宇谦.新生儿缺氧缺血性脑病CT与B超比较分析.影像诊断与介入放射学,1998；7：167.
22.谢礼逊,苏一媛,陈双.新生儿窒息缺氧缺血性脑病的CT诊断.中华放射学杂志,1993;27：236.
23.龙晚生,罗学毛,赵汝庸.新生儿缺氧缺血性脑病的CT随访观察.中华放射学杂志,1997;31：524.
24.陈旭生,林霓阳,房晓伟,等.新生儿缺氧缺血性脑病179例临床和CT的分析.新生儿科杂志,1999；14(3)：104.
25.龙晚生,罗学毛.新生儿缺氧缺血性脑病的CT随访观察.Chin J Radiol,1997;31(8)：524.
26.吴天,张翔,张云亭.新生儿缺氧缺血性脑病的临床与CT诊断.医学影像学杂志,1999；9(2)：129.
27.谢礼逊,苏一媛,陈双.新生儿窒息缺氧缺血性脑病的CT诊断.中华放射学杂志,1993；27(4)：237.
28.陈惠金.新生儿缺氧缺血性脑病和颅内出血的关系及鉴别.中国实用儿科杂志,1995;10(3)：83.
29.罗克娴,储宗瀛,李艳苓.71例新生儿窒息颅脑CT的观察.新生儿科杂志,1989；4(1)：6-7.
30.Schrumpt JD. Correlation of early neurzologic outcome and CT findings in neonatal brain hypoxia and injury. J Comput Assist Tomogr,1980; 4:445.
31.Schrumpf J D. Correlation of early neurologic outcome and CT findings in neonatal brain hypoxia and injury. J Com2 put Assist Tomogr,1980; 4:445
32.Brid CR. Pathophysiology of "reverse" edema in global cerebral ischemia. AJNR,1989; 10:95.
33. Brid CR. Pathophysiology of"reverse"edema in global cerebral ischemia. AJNR.1989; 10:95.
34.Lupton B A,Hill A,Roland E H.Brain swelling in the asphxxiated term newborn. pediatrics,1988; 82:139.
2.王慕狄.儿科学.五版.北京：人民卫生出版社,2001年.
3.马晓燕,刘永林.新生儿缺氧缺血性脑病63例颅脑CT诊断分析.实用医技杂志,2009年9月；16(9)：708—709.
4.李贵生.新生儿缺血缺氧性脑病的CT表现及治疗原则.实用医技杂志,2004年1月；11(1)：25.
5.张雪斌,周珉.CT在评价小儿颅内出血中的价值.实用医技杂志,2003年12月；10(12)：1353—1354.
6.刘玉花,姜山,肖格林.新生儿缺氧缺血性脑病的CT诊断.实用放射学杂志,2002年6月;18(6)：514—515.
7.金新安,蔡淑芳,姜锐松,敖振杰.早产儿与足月儿缺血缺氧性脑病的CT对照分析.实用放射学杂志,2001年6月；17(6)：462—464.
8.袁斌.新生儿缺血缺氧性脑病的CT诊断.江西医学院学报,2003；43(4)：54.
9.徐宗芳.599例患儿脑部疾病头颅CT的应用意义.临床儿科杂志,1996年；14(4)：256—257.
10.杨州,李莉媛,李健丁,张跃珍.CT检查在小儿癫痫诊断中的价值.中国医学影像技术,2003;19(2)：158—160.
11.李启桃,蔡毅勇,张家祥.64例新生儿缺血缺氧性脑病的CT诊断.上海医学影像杂志,1995;4(2)：84—86.
12.蒋敏.新生儿缺血缺氧性脑病CT应用价值.镇江医学院学报,1996,6(2)：150.
13.吕雷,米延,张丽杰,赵德超.新生儿脑疾病临床与CT诊断对照分析.哈尔滨医科大学学报,1994；28(6)：495、515.
14.李仰年,刘国瑞.磁共振成像在新生儿缺血缺氧性脑病中的应用.汕头大学医学院学报,2004;17(3)：190—192.
15.刘国瑞,方文辉,郑文斌,刘启则.MRI对新生儿缺氧缺血性脑病的分度诊断价值.影像诊断与介入放射学,2001；10(2)：71—73.
16.岳冬梅,毛健.足月新生儿缺氧缺血性脑损伤神经病理MRI评价.中华围产医学杂志,2005年3月;8(2)：134—135.
17.陈丽英.MRI与1 HMRS对足月新生儿缺氧缺血性脑病预后的判断.放射学实践,2000年1月;15(1)：57—59.
18.关计添,刘国瑞.磁共振波谱在新生儿缺血缺氧性脑病中的应用.汕头大学医学院 学报,2003;16(4)：233—235.
19.王芳,邵剑波,徐祖高.新生儿缺氧缺血性脑病后遗症的CT与MRI评价.]BIMONTHLY,2003JUN; 12 (3):105-108.
20.谢丽娟,陈惠金,陈冠仪.新生儿颅内出血的超声CT及MRI的诊断特性比较.中
国当代儿科杂志,2003年12月；5(6)：550—552.
21.曹巧玲,张善云.新生儿缺氧缺血性脑病MRI检查与临床分析探讨.海南医学,2002;13(4)：63.
22.明兵,李振勋,高源统,陈爱菊.新生儿窒息早期的MRI表现与预后的关系.中华放射学杂志,2002年7月：36(7)：637—640.
23.秦永春.磁共振成像在新生儿缺氧缺血性脑病中的应用.华北煤炭医学院学报,2001年7月；3(4)：464—465.
24.陈惠金,谢丽娟,陈冠仪,朱杰明.新生儿矢状区损伤的头颅MRI和CT的诊断特征.中华放射学杂志,2001年9月；35(9)：716—717.
25.龙晚生,罗学毛,梁长虹,李晓群.儿童脑室周围白质软化症的临床和MRI诊断.中华放射学杂志,1998年5月；32(5)：303—305.
26.G.K.Malik,M.Pandey,R.Kumar,S.Chawla,B.Rathi.MR imaging and in vivo proton spectroscopy of the brain in neonates with hypoxic ischemic encephalopathy. European Journal of Radiology 2002;43(2002):6-13.
1.韩玉昆,许植之,虞人杰.新生儿缺氧缺血性脑病.1版.北京：人民卫生出版社2000年.
2.王慕狄.儿科学.五版.北京：人民卫生出版社,2001年.
3.马晓燕,刘永林.新生儿缺氧缺血性脑病63例颅脑CT诊断分析.实用医技杂志,2009年9月；16(9)：708—709.
4.李贵生.新生儿缺血缺氧性脑病的CT表现及治疗原则.实用医技杂志,2004年1月;11(1)：25.
5.张雪斌,周珉.CT在评价小儿颅内出血中的价值.实用医技杂志,2003年12月;10(12)：1353—1354.
6.刘玉花,姜山,肖格林.新生儿缺氧缺血性脑病的CT诊断.实用放射学杂志,2002年6月；18(6)：514—515.
7.金新安,蔡淑芳,姜锐松,敖振杰.早产儿与足月儿缺血缺氧性脑病的CT对照分析.实用放射学杂志,2001年6月;17(6)：462—464.
8.袁斌.新生儿缺血缺氧性脑病的CT诊断.江西医学院学报,2003；43(4)：54.
9.徐宗芳.599例患儿脑部疾病头颅CT的应用意义.临床儿科杂志,1999年;14(4)：256—257.
10.杨州,李莉媛,李健丁,张跃珍.CT检查在小儿癫痫诊断中的价值.中国医学影像技术,2003；19(2)：158—160.
11.李启桃,蔡毅勇,张家祥.64例新生儿缺血缺氧性脑病的CT诊断.上海医学影像杂志,1995;4(2)：84—86.
12.蒋敏.新生儿缺血缺氧性脑病CT应用价值.镇江医学院学报,1996,6(2)：150.
13.吕雷,米延,张丽杰,赵德超.新生儿脑疾病临床与CT诊断对照分析.哈尔滨医科大学学报,1994;28(6)：495、515.
14.陈惠金,谢丽娟,陈冠仪,朱杰明.新生儿矢状区损伤的头颅MRI和CT的诊断
特征.中华放射学杂志,2001年9月；35(9)：716—717.
15.龙晚生,罗学毛,梁长虹,李晓群.儿童脑室周围白质软化症的临床和MRI诊断.中华放射学杂志,1998年5月;32(5)：303—305.
16.虞人杰.新生儿缺氧性脑病临床及CT诊断存在的问题.中国实用儿科杂志,
2000;15：340-341.
17.韩玉昆,虞人杰,卜定方.新生儿缺氧缺血性脑病临床诊断依据和分度.中华儿科杂志,1990；28：31.
18.韩玉昆,整理.新生儿缺氧缺血性脑病诊断依据和临床分度.中华儿科杂志,1997； 35：99.
19.龚金山,刘智勇,刘宝治.新生儿缺氧缺血性脑病的CT诊断.云鹤,王立平,高宝山.内蒙古自治区医学科学论文选编.呼和浩特：远方出版社,1998.117.
20.方红.CT"反转征”—儿童缺氧／缺血性脑损伤的结果.国外医学：临床放射学分册,1990：13：349.
21.方国涛,周世铮,周宇谦.新生儿缺氧缺血性脑病CT与B超比较分析.影像诊断与介入放射学,1998；7：167.
22.谢礼逊,苏一媛,陈双.新生儿窒息缺氧缺血性脑病的CT诊断.中华放射学杂志,1993;27：236.
23.龙晚生,罗学毛,赵汝庸.新生儿缺氧缺血性脑病的CT随访观察.中华放射学杂志,1997;31：524.
24.陈旭生,林霓阳,房晓伟,等.新生儿缺氧缺血性脑病179例临床和CT的分析.新生儿科杂志,1999；14(3)：104.
25.龙晚生,罗学毛.新生儿缺氧缺血性脑病的CT随访观察.Chin J Radiol,1997;31(8)：524.
26.吴天,张翔,张云亭.新生儿缺氧缺血性脑病的临床与CT诊断.医学影像学杂志,1999；9(2)：129.
27.谢礼逊,苏一媛,陈双.新生儿窒息缺氧缺血性脑病的CT诊断.中华放射学杂志,1993；27(4)：237.
28.陈惠金.新生儿缺氧缺血性脑病和颅内出血的关系及鉴别.中国实用儿科杂志,1995;10(3)：83.
29.罗克娴,储宗瀛,李艳苓.71例新生儿窒息颅脑CT的观察.新生儿科杂志,1989；4(1)：6-7.
30.Schrumpt JD. Correlation of early neurzologic outcome and CT findings in neonatal brain hypoxia and injury. J Comput Assist Tomogr,1980; 4:445.
31.Schrumpf J D. Correlation of early neurologic outcome and CT findings in neonatal brain hypoxia and injury. J Com2 put Assist Tomogr,1980; 4:445
32.Brid CR. Pathophysiology of "reverse" edema in global cerebral ischemia. AJNR,1989; 10:95.
33. Brid CR. Pathophysiology of"reverse"edema in global cerebral ischemia. AJNR.1989; 10:95.
34.Lupton B A,Hill A,Roland E H.Brain swelling in the asphxxiated term newborn. pediatrics,1988; 82:139.