目的 观察脑损伤早产儿血清25-羟维生素D[25-(OH)D]水平的变化情况,探讨其与炎症反应的关系.方法 选择生后24 h内入住NICU的53例早产儿,其中发生脑损伤24例(观察组),未发生脑损伤29例(对照组).采集两组生后第1、7、14天桡动脉血,采用ELISA法检测血清25-(OH)D及IL-17、IL-10水平,分析血清25-(OH)D与IL-17、IL-10的相关性.结果 两组血清25-(OH)D水平在生后第1、7天较低,第14天逐渐升高,观察组各时间点25-(OH)D水平均低于对照组(P均<0.05).观察组第7天IL-17水平高于第1、14天(P均<0.05),第14天与第1天差异无统计学意义(P>0.05),观察组各时间点IL-17水平均高于对照组(P均<0.05).观察组第14天IL-10水平高于第1、7天(P均<0.05),对照组IL-10水平第7天低于第1天、第14天低于第7天(P均<0.05).观察组血清25-(OH)D水平在生后第1、7、14天与IL-17水平均呈负相关(P均<0.05),在第1、7天与IL-10水平呈正相关(P均<0.05).结论 脑损伤早产儿生后各时间点血清25-(OH)D水平均较低,其水平变化与IL-17、IL-10水平相关;补充维生素D或可抑制脑损伤后的炎症反应.

目的 探讨血清血红素氧合酶-1(HO-1)、高迁移率族蛋白B1(HMGB1)在早产儿支气管肺发育不良(BPD)发病中的作用及近期神经系统发育评估中的价值.方法 选取2019年12月至2021年3月徐州医科大学附属医院新生儿重症监护室收治的96例早产儿作为研究对象.根据BPD诊断标准分为BPD组40例和非BPD组56例.根据矫正胎龄36周时需吸入氧浓度(FiO2)情况将BPD组分为轻度亚组(未用氧)、中度亚组(FiO2<30％)及重度亚组(FiO2≥30％或需机械通气).采用ELISA法检测两组早产儿出生后第1、7、14、28天血清HO-1、HMGB1水平,于出生后1周内及矫正胎龄40周时监测振幅整合脑电图(aEEG)评分.比较两组早产儿出生后第1、7、14、28天血清HO-1和HMGB1水平和出生后1周内及矫正胎龄40周时aEEG评分,同时分析BPD组早产儿血清HO-1、HMGB1水平与aEEG评分的相关性.结果 BPD组早产儿出生后第7、14、28天血清HO-1、HMGB1水平均高于非BPD组,差异均有统计学意义(均P<0.05);而两组早产儿出生后第1天血清HO-1、HMGB1水平比较差异均无统计学意义(均P>0.05).BPD轻度、中度及重度亚组早产儿出生后1周内、矫正胎龄40周时aEEG评分均低于非BPD组,差异均有统计学意义(均P<0.05);BPD中度及重度亚组早产儿出生后1周内、矫正胎龄40周时aEEG评分均低于轻度亚组,重度亚组早产儿出生后1周内、矫正胎龄40周时aEEG评分均低于中度亚组,差异均有统计学意义(均P<0.05).BPD组出生后第7天血清HO-1、HMGB1水平与出生后1周内aEEG评分均呈负相关(均P<0.01),出生后第7、14、28天血清HO-1、HMGB1水平与矫正胎龄40周时aEEG评分均呈负相关(均P<0.01).结论 HO-1、HMGB1可能与早产儿BPD的形成有关,并可能影响早产儿的近期神经系统发育.

目的 探究头颈部动脉夹层的临床特点,通过超声随访患者分析血管再通的情况.方法 对24例自2014年06月-2017年10月于我科诊断为急性脑梗死或TIA,而且经过检查确诊为头颈部动脉夹层的患者,对其临床特点以及治疗和随访进行了分析.结果 24例颈动脉夹层患者的发病高危因素包括近期上呼吸道感染、高血压、结缔组织疾病、颈部按摩、长期吸烟、颈部轻微外伤等.主要给予阿司匹林及氯吡格雷等药物治疗.在治疗后24例患者NIHSS评分均有所降低,并且在随访时没有发生新的缺血性脑卒中事件.在超声随访中,颈部血管中有7例(21.4％)发生再通,再通时间7日至6月不等.结论 颈部动脉夹层的临床表现多样,是青年脑梗死的常见病因,应高度警惕.药物治疗是目前颈部动脉夹层的首选治疗方案,其再通率的影响因素尚不十分明确,需更为严密的研究方案来进行研究.

Objective To investigate the clinical and molecular biological features of spinocerebellar ataxia type1 (SCA1) . Methods A total of 8 members of a SCA1 family were tested ,of which 4 people were clinical positive patients and the rest were asymptomatic. The clinical manifestations , imaging and electrophysiological findings of the family members were analyzed.PCR-STR was used to detect the abnormal CAG trinucleotide expansion in ATXN1. Results The abnormal CAG trinucleotide expansion in ATXN1 were detected in the 8 people. The initial manifestation of the 4 patients were progressive cerebellar ataxia , mainly manifested as gait disturbance , difficulty in walking and accompanied with dysarthria , dysphagia and up-gaze palsy. Neuropathological studies revealed cerebellum and brain stem atrophy. Neuroelectrophysiological examination showed different degrees of abnormalities , especially in the 4 patients with positive clinical symptoms. Conclusions SCA1 is inherited in an autosomal dominant manner. Progressive cerebellar ataxia and bulbar dysfunction are common. The diagnosis of SCA1 rests on the result of molecular genetic testing and clinical characteristics.

Objective Analysis of multiple system atrophy clinical manifestations,imaging and electromyography of anal sphincter,sympathetic skin reaction examination results,explore the value of EAS-EMG and SSR for early clinical diag-nosis of MSA.Methods Retrospective analysis which were treated in Fifth Affiliated Hospital of Zhengzhou University from January 2015 to June 2017,and analysis of the complete data MSA outpatient and inpatients with a total of 32 cases,20 pa-tients with MSA-P,12 patients with MSA-C.All patients were admitted to hospital after head of routine magnetic resonance imaging (MRI) and anal sphincter electromyography,sympathetic skin response,the general data of MSA patients,MRI, neural electrophysiological results were statistically analyzed.Results Among the 32 patients,MSA-P type 20 cases,the main clinical manifestations were Parkinson-like symptoms,MSA-C type 12 cases,the main clinical manifestations of cere-bellar ataxia.32 patients underwent routine magnetic resonance imaging,and 28 presented MRI abnormalities.The fissure sign of the putamen in the T2WI sequence was mainly seen in type MSA-P(P<0.05),whereas the pontine cross sign was mainly seen in type MSA-C (P<0.05).30 patients with MSA underwent EAS-EMG examination,and 28 patients showed neurogenic damage.The main manifestation was the prolongation of the motor unit potential(MUPs),the prolongation of the average time,the increase of the multi-phase wave,and the occurrence of the satellite potential.31 patients with MSA under-went SSR examination,and 27 patients showed autonomic nerve dysfunction.The main finding was the prolongation of the initial latency and the absence of waveform.Conclusion Combined with clinical features,craniocerebral conventional mag-netic resonance examination results and EAS-EMG,SSR examination,can improve the diagnostic rate of MSA.When EAS-EMG examination is limited,SSR examination can provide supplementary diagnosis and reliable reference.

目的 观察脑动脉夹层致缺血性脑卒中患者的临床资料,分析其发病机制,为临床诊断和治疗方案提供有效参考.方法 选取30例脑动脉夹层致缺血性脑卒中的患者,按照夹层发生的位置将其分为颅内组和颅外组,对其临床资料进行回顾性分析和对比,对比两组患者的影像学表现和梗死机制.结果 颅内组与颅外组的影像学表现之间无统计学意义的差异(P>0.05),在梗死机制的比较上,两组单纯梗塞性梗死的组间差异具有统计学意义(P<0.05),而在单纯穿支闭塞性梗死、栓塞+穿支闭塞性梗死以及栓塞+血流动力性梗死的组间差异上均无统计学意义(均P>0.05).结论 在脑动脉夹层中,颅外段夹层所占比例较大,颅外段脑动脉夹层多由单纯栓塞导致缺血性脑卒中,而颅内段脑动脉夹层则少见由单纯栓塞所致的缺血性脑卒中,且颅内颅外均可能由其他机制引起梗死.