小儿颅脑疾病与头颅计算机断层成像术

目的 探讨头颅ＣＴ检查在小儿颅脑疾病诊断中的重要意义。方法 以３７０例头颅ＣＴ异常的非外伤性病变的患儿为研究对象,按疾病增将其归类、比较、分析,从中揭示其关系。结果 各类癫痫的主要ＣＴ改变是脑萎缩,脑软化次之;小儿颅脑肿瘤以幕下、中线部位多见,颅高压征出现象,定位体征少见,易于误诊;新生儿颅脑损伤发病率高,头颅ＣＴ检查得于新生儿缺氧缺血性脑病和新生儿颅内出血的诊断。结论 头颅ＣＴ是小儿颅脑疾病的首选检查方法,安的应用使颅脑疾病的诊断水平明显提高。     

头颅X线片在颅脑损伤诊断中的应用价值

医学影像技术的飞速发展，CT在颅脑损伤中普遍应用，动态CT检查成为颅脑损伤患者的首选方法，故有些医生就忽略了X线检查在颅脑损伤中的作用，从而导致漏诊，甚至延误病情的救治。通过回顾性分析我院2001年脑外科成立至2004年10月颅脑损伤后头颅CT扫描检查和头颅X线片检查颅骨骨折诊断结果，进一步探讨头颅X线片在颅脑损伤诊断中的应用价值。     

CT检查对儿童急性颅脑外伤的诊断价值

目的分析儿童急性颅脑外伤诊断中CT检查方式的应用效果。方法选取急性颅脑外伤患儿100例,随机分为两组,对照组行常规剂量CT检查,观察组行低剂量CT检查,对比两组扫描辐射剂量、头颅病变情况。结果与对照组对比,观察组DLP、CTDIw更低,差异明显,P 0. 05。两组患者术后病理诊断结果完全一致,诊断符合率为100%。结论儿童急性颅脑外伤诊断中低剂量CT检查方式的应用效果显著,可推广。     

增强CT对小儿结核性脑膜炎的临床诊断价值探究

目的：探究增强CT对小儿结核性脑膜炎的临床诊断价值。方法选择2012年1月~2013年1月来我院诊治结核性脑膜炎患儿的120例为本次研究对象,对其进行头颅CT及增强CT检查、MRI检查和CSF检查。结果利用头颅CT及增强CT对小儿结核性脑膜炎进行检查,具有较高的有效率,且对患儿的病情及病理有了全面掌握,具有典型性和可比性(P<0.05);利用MRI检查有效率相对较差,不具备典型性,而运用CSF虽然能够全面掌握患儿病情,但在典型性上还有所欠缺。结论通过增强CT对小儿结核性脑膜炎的临床诊断,能够对患儿的并且进行有效掌握,应与原有的检查方式相配合,从而确保临床诊断的客观全面性,为患儿的治疗奠定基础。     

新生儿头颅B超300例临床分析

目的为探讨我省新生儿头颅B超筛查对象.方法使用东芝SSA-240A 型超声诊断仪,对我院分娩及NICU住院的新生儿随机抽取早产儿、高危新生儿、正常新生儿各100例(共300例)行新生儿头颅B超检查,采用SPSS统计分析软件进行χ2及t检验.结果①三组间颅脑损伤顺序是早产组＞高危组＞正常组,发生分别为63%(63/100)、20%(20/100)、4%(4/100),P＜0.01;②与颅脑损伤关系密切的因素有:早产及低体重儿、新生儿窒息、肌张力改变、呼吸改变、缺氧及酸中毒;③早产组、高危组的组内颅脑损伤与正常各因素均无明显差异.结论提示早产儿、高危新生儿中颅脑损伤发生率高且无特异性,应早期常规行B超颅内检查,以便早期诊断和及时治疗,降低颅脑病变患儿的病死率及后遗症的发生率,减少伤残儿.     

84例新生儿缺氧缺血性脑病头颅CT与临床分析

新生儿缺氧缺血性脑病(HIE),为围产期窒息而导致的脑损伤的主要原因,虽然由于产、儿科重症监护技术发展,使围产期病死率有所降低,但HIE发生率仍然较高.后遗症的发生率均较高,临床上早期诊断及头颅CT检查时对HIE的诊断,早期治疗,对HIE的预后有重要意义.现将我院1996年～2000年住院的新生儿HIE已做头颅CT检查的84例患儿分析如下.     

闪光视觉诱发电位无创颅内压监测结合头颅CT的临床研究

目的:探讨闪光视觉诱发电位无创颅内压监测与头颅CT之间的相关性.方法:用无创颅内压监测仪对50例颅脑外伤患者进行动态颅内压监测,其中重型颅脑损伤者20例,中型23例,轻型7例;每次检测后行头颅CT检查并计分,分析其CT变化特征,并与颅内压值对照.结果:伤后同一时点,患者的颅内压和头颅CT计分比较,重型＞中型＞轻型(P＜0.05).中、重型颅脑损伤患者保守治疗组和手术治疗组的颅内压与头颅CT计分之间,组内比较具有相关性,计算相关系数分别为r=0.92和r--0.96,差异有统计学意义(P＜0.05).结论:闪光视觉诱发电位无创颅内压监测与头颅CT变化呈正相关,两者结合可以指导治疗并判断预后.     

新生儿头颅血肿与新生儿颅内损伤的关系(附254例报告)

本文选择1995年至2003年6月本院诊断为新生儿头颅血肿254例,总结分析发现新生儿头颅血肿半数合并颅内损伤,如新生儿缺氧缺血性脑病(HLE)、颅内出血。提示对新生儿头颅血肿病人应仔细查体,及时进行影像学检查,如颅脑CT、B超、MRI等,进行NBNA评分,以明确颅内病变,及早干预治疗。本病预后与颅内损伤程度有关。临床资料 病例来源:本院自1995年至2003年6月收治头颅血肿254例。男195例,女59例;年龄为生后30min至27d的新生儿。其中>37w35例,37-43w158例,<43w61例;体重<2500g51例,2500-4000g158例,<4000g45例。 临床表现:意识改变30例,激惹71例,呼吸异常94例,     

新生儿颅内出血120例病例分析与CT检查

新生儿颅内出血是新生儿期最常见的严重疾病,也是新生儿死亡的主要原因之一。其特点为病情凶险,死亡率高,存活者有不同程度的后遗症。本病靠临床诊断有时易误诊漏诊。应用头颅CT检查明显提高了诊断率,及早合理治疗,明显减少了病死率及后遗症的发生率,减轻后遗症程度。现将我院1     

神经生长因子与血管内皮生长因子在新生儿缺氧缺血性脑病中的关系

目的 探讨神经生长因子治疗新生儿缺氧缺血性脑病的机制及有效方案.方法 选择我院2004年3月～2007年3月本院新生儿病房生后3天内符合全国HIE诊断标准13J的患儿82例随机分为对照组和观察组,分别于住院当天、住院3天和住院7天分别进行血浆血管内皮生长因子、CT检查及B超检查;以及进行NBNA20项行为测定和神经精神发育随访.结果 观察组与对照组治疗后显示肌张力、吸吮反射、拥抱反射和意识恢复时间比较有显著差异.观察组与对照组患儿颅脑B超住院3天比较脑水肿指标有极显著差异.观察组、对照组患儿血浆血管内皮生长因子与同组0天比较有显著差异.观察组与对照组小儿颅脑CT异常率住院3天、住院7天比较有显著差异.观察组与对照组小儿住院7天、住院28天NANB评分结果比较有统计学意义.6个月时随访,观察组与对照组小儿精神运动发育商有显著差异.结论 外源性神经生长因子可以使受损的神经元得以修复,而在新生儿缺血缺氧性脑病的早期由于血管内皮生长因子的水平较高,不宜使用.     

Cerebral malaria

Cerebral malaria is a rapidly progressive potentially fatal complication of Plasmodium falciparum infection. It is characterized by unarousable and persistent coma along with symmetrical motor signs. Children, pregnant women and non-immune adults are more susceptible to have cerebral malaria. Several clinical, histopathological and laboratory studies have suggested that cytoadherence of parasitized erythrocytes (mechanical hypothesis), and neuronal injury by malarial toxin and excessive cytokine (e.g. tissue necrosis factor-alpha) production (cytotoxic hypothesis) are possible pathogenic mechanisms. Several associated systemic complications like hypoglycemia, hypovolemia, hyperpyrexia, renal failure, bleeding disorders, anemia, lactic acidosis and pulmonary oedema may contribute in the pathogenesis of coma, and are responsible for high mortality. The meticulous supportive care along with intravenous administration of antimalarial drugs are corner-stone of the treatment. Quinine is currently, drug of choice. Artimisinin derivatives are equally effective and can be used by intramuscular route. In severe cases exchange blood transfusion may be an effective alternative. Corticosteroids has no place in the management of cerebral malaria. The occurrence of convulsions are common in children, these can be prevented with the use of single intramuscular administration of phenobarbitone. Despite advances in the management mortality and morbidity have not changed much. A large number of surviving patients are left with permanent neurological sequelae. There is a need to search for effective malaria prevention and interventional strategies to avert high mortality and morbidity associated with cerebral malaria.     

Cerebral ganglioglioma

Summary The morphological characteristics of neurons revealed by Golgi's method are reported in a case of cerebral ganglioglioma.Spindle-shaped (leptodendritic) neurons and radiated type I neurons form the bulk of this tumour. According to Ramon-Moliner (1968) isodendritic neurons (both leptodendritic and radiate type I) are philogenetically primitive cells and differ greatly from those observed in most of the deep cerebral nuclei of the mammalian's brain.     

Cerebral vasospasm

Cerebral vasospasm (specifically, intracranial arterial spasm) is variously defined as: (1) an arteriographically evident narrowing of the lumen of one or more of the major intracranial arteries at the base of the brain due to contraction of the smooth muscle within the arterial wall, or due to the morphological changes in the arterial wall and along its endothelial surface that occur in response to vessel injury; (2) the delayed onset of a neurological deficit following subarachnoid hemorrhage, thought to be due to ischemia or infarction of a portion of the brain; or (3) the combination of these two features (symptomatic vasospasm). The arterial contraction of intracranial arterial spasm typically develops a few days after the rupture of an intracranial aneurysm and lasts 2 to 3 weeks. Such arterial spasm can also occur in other conditions such as head trauma. If it is severe enough it can lead to cerebral infarction. The pathogenesis of this condition is still unclear. Many ingenious attempts have been made to prevent or treat cerebral vasospasm, but most have failed. The best current approach is to ensure adequate blood volume, and to elevate the patient's blood pressure (especially if the aneurysm has been secured by an early operation). The continuing investigation of drugs such as calcium channel blocking agents to improve the cerebral circulation has begun to provide additional help.     

Cerebral Malaria

Malaria infection of the Central Nervous System (CNS) can cause a severe neurological syndrome termed Cerebral Malaria (CM). The central neuropathological feature of CM is the preferential sequestration of parasitised red blood cells (PRBC) in the cerebral microvasculature. The level of sequestration is related to the incidence of cerebral symptoms in severe malaria. Other neuropathological features of CM include petechial hemorrhages in the brain parenchyma, ring hemorrhages and Diirck's granuloma's. Immunohisto-chemical and electron microscopy studies have shown widespread cerebral endothelial cell activation and morphological changes occur in CM, as well as focal endothelial cell damage and necrosis. The immune cell response to intravascular sequestration appears to be limited, although activation of pigment-phagocytosing monocytes is a late feature. The mechanisms by which PRBC cause coma in malaria remain unclear. In vitro parasitised erythrocytes bind to endothelial cells by specific, receptor mediated interactions with host adhesion molecules such as ICAM-1, whose expression on cerebral endothelial cells is increased during CM as part of a systemic endothelial activation. Induction of local neuro-active mediators such as nitric oxide and systemic cytokines like TNFα may be responsible for the rapidly reversible symptoms of the coma of CM. The recent cloning of the parasite ligand PfEMP-1, thought to mediate binding to host sequestration receptors, promises further insight into the relationship between patterns of sequestration and the incidence and pathogenesis of coma in cerebral malaria.