BAEP转颈试验对VBI诊断价值的研究

目的：研究脑干听觉诱发电位（BAEP）转颈试验对椎基底动脉供血不足（VBI）的诊断价值。方法：对临床诊断为VBI而普通BAEP，TCD检查阴性的32例病人，作BAEP转颈试验。结果：？BAEP阳性率为37．5％，结论：BAEP转颈试验可提高VBI病人的阳性检出率。     

BAEP对新生儿及婴幼儿听力检测的价值

目的探讨脑干听觉诱发电位（BAEP）对新生儿及婴幼儿听力检测的价值。方法运用脑干听觉诱发电位（BAEP）检测48例出生后用美国产“GST听力筛查仪”筛查未通过的新生儿及婴幼儿进行听力测定。结果48例患儿BAEP示，总异常率为45例（占93．75％），其中37例为听力异常伴BAEP异常（占77．08％），以轻、中度耳聋多见（共30例，50耳次）；中度以上有7例（共14耳次）；有8例有BAEP异常但无听力异常者（占16．67％）；3例听力及BAEP均正常（占6．25％）。结论BAEP能鉴别新生儿及婴幼儿“听力初筛未通过”的患儿是因耳蜗感音性听力障碍还是脑干听觉传导通路上的异常引起，从而判断耳聋的程度及性质，为临床诊断和治疗的疗效评估提供可靠的依据。     

后循环短暂脑缺血发作患者BAEP及BR检测报告分析

目的探讨脑干听觉诱发电位（BAEP）和瞬目反射（BR）检查对于后循环短暂脑缺血发作患者脑干功能受损的诊断价值。方法选择66例后循环短暂脑缺血发作患者（TIA组），分别行BAEP和BR检查，观察BAEP波形及各波潜伏期（PL）、峰间潜伏期（IPL），计算BR各成分平均潜伏期，并与40例健康者作对照。结果TIA组中BAEP检出脑干异常48例（72.7％），BR检出脑干异常50例（75.8％），两者联合检测脑干异常60例（90.9％）。结论BAEP与BR均能敏感地反映脑干的病变，两者从不同的解剖路径反映了脑干病变的病理生理基础，有助于定位诊断。     

MRI和BAEP在多系统萎缩下不同类型中的诊断价值

目的：探讨多系统萎缩（MSA）的临床,, 以及磁共振成像（MRI）和脑干听觉诱发电位（BAEP）对不同类型MSA的诊断价值。方法：对50例MSA的临床资料,MRI和BAEP进行回顾性分析,结果：50例MSA中,散发型橄榄桥脑小脑萎缩（SOPCA）25例,占50．0％,临床上以小脑型共济失调为主要表现,BAEP最敏感,MRI次之;纹状体黑质变性（SND）15例,占305,以肌张力增高为主,MRI最敏感,BAEP次之。Sy-drager综合（SDS）10例占20％,以直立性低血压和头晕为主,BAEP最敏感,而且将SND与原发性帕金森综合征（IPD）的BAEP相比,前者的敏感性明显升高,差别有显著性。结论：MSA分型不同临床表现各有侧重,MRI及BAEP在MSA诊断和鉴别诊断中有极重要价值。     

脑干听觉诱发电位对癫痫患儿检测的意义

目的探讨脑干听觉诱发电位在癫痫患儿检测中的意义。方法对2000—01～2008—01我院38例癫痫患儿BAEP的检狈5结果进行总结。结果BAEP正常15例（39．5％），异常23例（60．5％），其中21例BAEP改变形式多样，异常指标相混出现。结论癫痫患者存在脑干功能异常。     

TCD、BAEP对椎—基底动脉供血不足的诊断价值

本文对110例椎基底动脉供血不足患者进行了TCD、BAEP的双重检测研究，结果显示在缺血发作期，两者的异常率分别是97．1％和90％（P＞0．05）;缓解期两者的异常率分别为88．2％和63．1％。本研究证实TCD、BAEP能准确、快捷的对椎基底动脉供血不足诊断，阳性率高，有极高的诊断价值。     

脑干听觉诱发电位对脑干缺血诊断价值的探讨

目的：探讨脑干听觉诱发电位对脑干缺血诊断价值。方法：对44例经颅多普勒检查（TCD）确定为椎基底动脉供血不足的眩晕患者（VBI组）进行脑干听觉诱发电位（BAEP）检查,并与52例经颅多普勒检查确定为脑血管痉挛的眩晕患者（对照组）脑干听觉诱发电位检查结果进行对照分析。结果：椎基底动脉供血不足的眩晕组BAEP异常率为52．27％,明显高于对照组（3．85％,P＜0．001）。VBI组BAEP各波潜伏期均长于对照组（P＜0．05）,BAEP的I波及V波波幅低于对照组（P＜0．05）。结论：脑干听觉诱发电位可作为评价脑干缺血及其程度的一个客观指标。     

脑干听觉诱发电位改变对Binswanger病的评估价值

目的用脑干听觉诱发电位方法检测Binswanger病的脑功能改变。方法对20例BD病患者、20例非痴呆脑血管病患者、20例老年健康人同时进行脑干听觉诱发电位（BAEP）检查。结果BAEP异常：BD病10例（50％），非痴呆脑血管病2例（10％），经统计学检查BD组BAEP与健康组、非痴呆脑血管病组有显著性差异，非痴呆脑血管病组与健康组无显著性差异。结论BAEP异常反应BD病患者有脑干功能受损和弥漫性脑功能障碍，并可作为BD病患者脑功能损害检查敏感指标，以及与非痴呆脑血管病患者鉴别诊断的一个辅助检查方法。     

脑干听觉诱发电位对新生儿高胆红素血症检测的临床意义

目的：通过脑子听觉诱发电住（BAEP）对新生儿高胆红素血症的测定，了解高胆红素对新生儿中枢神经系统的损害。方法：采用ZABR－200型脑干反应别听仪对100例新生儿高胆红素血症进行检查，并以30例新生儿肺炎作对照现查。结果：两组相比，X~2＝MM，P＜0．001观察组BAEP正常42例（42％），异常58例（58％）。结论：不同程度高胆红素血症均可引起中枢神经系统损害，胆红素越高BAEP异常率越高，且异常程度越重。BAEP敏感性高，影响因素小，结果准确可靠，为胆红素听觉传导通路神经毒性作用的判断指标。     

CT、核磁共振、诱发电位对多发性硬化的临床诊断价值

目的探讨CT、核磁共振（MRI）、诱发电位检查在多发性硬化（MS）临床诊断中的应用价值。方法对60例MS患者CT、核磁共振（MRI）、诱发电位检查结果与临床对比分析、结果MRI检查异常率最高．为85．1％，CT为41．7％．VEP为60％，SSEP为54．2％，BAEP为45．8％。如同时进行两项以上诱发电位检查．只要一项异常即判断为诱发电位异常，其异常率可达81．4％、结论CT、MRI、诱发电位检查结合应用可提高MS诊断的准确性。     

Regulatory Mechanism of MicroRNA-30b on Neonatal Hypoxic-Ischemic Encephalopathy (HIE)

ObjectiveThis study is to investigate the role of microRNA (miR)-30b in the pathogenesis of hypoxic-ischemic encephalopathy (HIE) in neonates.MethodsTotally 26 cases of neonatal HIE were included in this study. The protein expression levels of CD26P and PAI-1 were detected with ELISA. Serum levels of miR-30b and PAI-1 mRNA was measured by quantitative real-time PCR. Human brain microvascular endothelial cells (HBMECs) were cultured under hypoxic condition, and the intracellular expression levels of miR-30b and PAI-1 were evaluated. Dual-luciferase reporter assay was performed to confirm the interaction between miR-30b and PAI-1.ResultsCompared with the control group, both the mRNA and protein expression levels of PAI-1 in the serum were up-regulated in the neonates with HIE, together with up-regulated serum CD26P levels. However, the serum expression level of miR-30b was down-regulated in neonatal HIE. In hypoxia-induced HBMECs, the mRNA and protein expression levels of PAI-1 were significantly up-regulated, while the miR-30b expression level was significantly down-regulated. Dual-luciferase reporter assay showed that PAI-1 was the direct target of miR-30b.ConclusionNeonatal HIE is accompanied with abnormal platelet activation, significantly up-regulated serum PAI-1 expression levels, and down-regulated miR-30b expression. MiR-30b might regulate the disease pathogenesis and immune responses via modulating PAI-1.     

神经节苷脂GM1治疗新生儿缺氧缺血性脑病30例疗效观察

目的 探讨神经节苷脂GM1治疗新生儿HIE的疗效.方法 将60例HIE新生儿按照有无接受神经节苷脂GM1治疗分为治疗组和对照组各30例,比较2组治疗前后的神经行为评分(NBNA).结果 治疗组生后20 d时NBNA评分较对照组明显升高(25.700±2.706 vs 21.833±2.214),差异具有统计学意义.结论...     

神经电生理监测桥小脑角手术的研究(附106例报告)

目的探讨桥小脑角(CPA)手术中行神经电生理监测的意义。方法对106例CPA肿瘤病人进行了术中神经电生理监测,主要包括面神经、三叉神经、后组颅神经以及健侧脑干听觉诱发电位(BAEP)监测,观察术后面神经功能及并发症。结果面神经解剖保留96例(91%),面神经功能Ⅰ、Ⅱ级57例(54%),Ⅲ、Ⅳ级42例(40%),Ⅴ、Ⅵ级7例(6%)。术中健侧BAEP变化最明显的是Ⅲ～Ⅴ、Ⅰ～Ⅴ峰间潜伏期。结论在CPA手术中,采用诱发电位、肌电图实时监测,可及时为术者提供脑干功能的情况;术中健侧BAEP的Ⅰ～Ⅴ、Ⅲ～Ⅴ峰间潜伏期是重要监测指标;术中肌电图监测可以提示颅神经的位置和走行,为手术时避免损伤神经提供依据。     

单唾液酸四己糖神经节苷酯治疗新生儿缺氧缺血性脑病90例

目的研究单唾液酸四己糖神经节苷酯(GM1)静滴治疗新生儿缺氧缺血性脑病(HIE)疗效。方法将90例HIE患儿随机分为观察组和对照组,每组45例,均予常规治疗,观察组加用GM1。观察和记录2组临床症状、体征恢复情况和新生儿行为神经测定(NBNA)评分。结果应用GM1治疗新生儿HIE对改善HIE所致的远期神经系统发育障碍有较好的疗效。结论在常规治疗基础上加用GM1是目前治疗中重度HIE较理想的方法。     

脑干听觉诱发电位对癫(癎)患儿检测的意义

目的探讨脑干听觉诱发电位在癫患儿检测中的意义。方法对2000-01~2008-01我院38例癫患儿BAEP的检测结果进行总结。结果BAEP正常15例(39.5%),异常23例(60.5%),其中21例BAEP改变形式多样,异常指标相混出现。结论癫患者存在脑干功能异常。     

脑干听觉诱发电位检测对儿童颅内压增高的诊断意义

目的探讨脑干听觉诱发电位(brainstem anditory evoked potential,BAEP)在儿童颅内压(incranium pressure,ICP)增高诊断中的作用。方法本文采用MEB-9100型脑干诱发电位仪对颅内压增高患儿50例进行脑干听觉诱发电位检查。结果脑干诱发电位正常21例(42.0%),异常29例(58.0%)。结论脑干听觉诱发电位无损伤、可重复、波形稳定、不受意识状态及镇静剂影响、客观性强,可为儿童颅内压增高的临床诊断提供科学依据,对评价预后、指导治疗有一定的临床意义。     

神经节苷脂联合丹参注射液在新生儿缺氧缺血性脑病中的应用

目的探讨丹参注射液联合神经节苷脂的作用机制及其在新生儿缺氧缺血性脑病(HIE)中的应用效果。方法将我院确诊的HIE患儿80例随机分为治疗组(40例)和对照组(40例)。治疗组接受常规治疗及神经节苷脂与丹参注射液联合治疗,对照组进行常规治疗与神经节苷脂治疗。经10d治疗后评定治疗效果,统计病死率及临床表现恢复时间,分析2组治疗前后NABA评分、CT值。结果治疗组总有效率、NABA评分及CT值均明显高于对照组,而治疗组病死率、原始反射、意识状态及肌张力的恢复时间均低于对照组(P0.05)。结论神经节苷脂与丹参注射液治疗HIE有效率高、不良反应少、脑神经功能恢复快。     

Development of epilepsy in newborns with moderate hypoxic-ischemic encephalopathy and neonatal seizures

Background: Hypoxic-ischemic encephalopathy (HIE) is one of the most frequent causes of neonatal death or neurological handicaps such as cerebral palsy, mental delay, and epilepsy. Moreover, an acute consequence of HIE are neonatal seizures which can cause an additional brain damage. The neurodevelopmental outcome is known in the mild or severe cases of HIE, but in the moderate conditions the predictivity results, to date, unsatisfying. Objective: The purpose of this prospective study was to appraise the development of post-neonatal epilepsy in a cohort of term infants with moderate HIE and neonatal seizures. Methods: This study considered all newborns admitted to Neonatal Intensive Care Unit of the University of Parma between January 2000 and December 2002 for perinatal asphyxia, then followed by Neonatal Neurology Service. In all patients, neonatal variables such as type of delivery, birth weight, gestational age, Apgar scores, the need for resuscitation and assisted ventilation soon after birth, and arterial-blood pH were analyzed. Results: Ninety-two newborns were enrolled in the study because of perinatal asphyxia. Of these, 27 subjects developed mild HIE, 25 moderate, and five severe HIE. Neonatal seizures were present in 13 subjects with moderate HIE and in all newborns with severe HIE. At the last follow-up, only three infants belonging to patients with severe HIE developed epilepsy. Conclusion: Moderate HIE seems not to be related to post-neonatal epilepsy either if associated or not with neonatal seizures.     

Myelination patterns on magnetic resonance of children with developmental delay.

Magnetic resonance (MR) imaging was performed in 30 children with unexplained developmental delay who had associated neurological abnormalities such as seizures, spasticity, hypotonia, ataxia or poor vision. No child had a history of regression, preterm birth or neonatal cerebral injury. CT scans were performed before MR in all cases and were either normal or showed only mild atrophy. At least two MR sequences were obtained for all patients. Nine children had delayed or absent myelination on MR, one had patchy white-matter abnormalities, and in one patient myelination was topographically normal, but of inappropriately low signal intensity. MR was abnormal in six of seven children who had abnormal brainstem auditory evoked potentials (BAEP), and was normal in nine of 11 patients who had a normal BAEP. MR may have a useful r?le in demonstrating abnormal white-matter maturation in children with unexplained neurodevelopmental delay, particularly when abnormalities are found on BAEP studies.     

Neonatal hypoxic–ischemic encephalopathy reduces c-Fos activation in the rat hippocampus: evidence of a long-lasting effect

The effect of neonatal hypoxic–ischemic encephalopathy (HIE) on maturation of nociceptive pathways has been sparsely explored. To investigate whether neonatal HIE alters neuronal activity, nociceptive behavior, and serum neuroplasticity mediators (brain-derived neurotrophic factor [BDNF] and tumor necrosis factor-α [TNF]) in the short, medium, and long term. Neonate male Wistar rats were randomized to receive a brain insult that could be either ischemic (left carotid artery ligation [LCAL]), hypoxic (8% oxygen chamber), hypoxic–ischemic (LCAL and hypoxic chamber), sham-ischemic, or sham-hypoxic. Neuronal activity (c-Fos activation at region CA1 and dentate gyrus of the hippocampus), nociceptive behavior (von Frey, tail-flick, and hot-plate tests), neuroplasticity mediators (BDNF, TNF), and a cellular injury marker (lactase dehydrogenase [LDH]) were assessed in blood serum 14, 30, and 60 days after birth. Neonatal HIE persistently reduced c-Fos activation in the ipsilateral hippocampal region CA1; however, contralateral c-Fos reduction appeared only 7 weeks after the event. Neonatal HIE acutely reduced the paw withdrawal threshold (von Frey test), but this returned to normal by the 30th postnatal day. Hypoxia reduced serum LDH levels. Serum neuroplasticity mediators increased with age, and neonatal HIE did not affect their ontogeny. Neonatal HIE-induced reduction in neuronal activity occurs acutely in the ipsilateral hippocampal region CA1 and persists for at least 60 days, but the contralateral effect of the insult is delayed. Alterations in the nociceptive response are acute and self-limited. Serum neuroplasticity mediators increase with age, and remain unaffected by HIE.