The management of arteriovenous malformations in children

Between January 1941 and June 1989, 46 children below the age of 18 with an arteriovenous malformation (AVM) were managed. There were 7 patients with AVM diagnosed before the age of 2; 10 patients were diagnosed between the ages of 3 and 10; and 29 patients were diagnosed between 11 and 18. There were equal numbers of male and female patients. Twenty-five of the AVMs were large (>5 cm longest diameter). All 7 AVMs diagnosed before the age of 2 were large. The usual clinical presentation was congestive heart failure, bruit and an enlarging head. Three patients underwent excision with 2 deaths and 1 excellent result. In 11 patients (aged 3–18) with AVM without history of hemorrhage, 3 had excision with 2 excellent and 1 fair result. Four remained stable. Four developed progressive deficits or hemorrhage. In 10 patients (aged 3–18) with AVM and hemorrhage who were treated medically, 7 (70%) had an episode of re-hemorrhage. Three patients had excision of AVM after re-hemorrhage, but before the age of 18 with an excellent result. Eighteen patients (aged 3–18) with AVM and a single episode of hemorrhage underwent excision with 17 excellent or good results and 1 fair result. The overall mortality was 7%. Eighty-five percent of the children with excision of AVM had an excellent or good result. The best treatment for AVM in children is surgical excision.Presented at the XVII Annual Meeting of the International Society for Pediatric Neurosurgery, Bombay 1989     

Quantitative MRI of the brain in children with sickle cell disease reveals abnormalities unseen by conventional MRI

Conventional MRI (cMRI) has shown that brain abnormalities without clinical stroke can manifest in patients with sickle cell disease (SCD). We used quantitative MRI (qMRI) and psychometric testing to determine whether brain abnormalities can also be present in patients with SCD who appear normal on cMRI. Patients 4 years of age and older with no clinical evidence of stroke were stratified by cMRI as normal (n = 17) or abnormal (n = 13). Spin-lattice relaxation time (T1) of gray and white matter structures was measured by the precise and accurate inversion recovery (PAIR) qMRI method. Patient cognitive ability was assessed with a standard psychometric instrument (WISC-III or WISC-R). In all 30 patients with SCD, qMRI T1 was lower than in 24 age- and race-matched controls, in cortical gray matter (P < .0006) and caudate (P < .0009), as well as in the ratio of gray-to-white matter T1 (P < .008). In the 17 patients who were shown to be normal by cMRI, qMRI T1 was still lower than in controls, in both cortical gray matter (P < .02) and caudate (P < .004). Histograms of voxel T1 show that the proportion of voxels with T1 values intermediate between gray and white matter (ie, consistent with encephalomalacia) was 9% higher than controls in patients shown to be normal by cMRI (P < .05) and 15% higher than controls in patients shown to be abnormal by cMRI (P < .0005). The full scale intelligence quotient (FSIQ) of all patients with SCD was 75, compared to the FSIQ of 88 in a historical control group of patient siblings (P < .001). The FSIQ of patients shown to be normal by cMRI was 79, significantly lower than the FSIQ of patient siblings (P < .04). The FSIQ of 71 in patients shown to be abnormal by cMRI was significantly lower than both the patient siblings (P < .005) and the patients shown to be normal by cMRI (P < .04). Patients shown to be abnormal by cMRI scored lower than patients shown to be normal by cMRI, specifically on the subtests of vocabulary (P = .003) and information (P = .03). Cognitive impairment is thus significant, even in patients with SCD who were shown to be normal by cMRI, suggesting that cMRI may be insensitive to subtle neurologic damage that can be detected by qMRI. Because cognitive impairment can occur in children normal by cMRI, our findings imply that prophylactic therapy may be needed earlier in the course of SCD to mitigate neurologic damage.     

核苷酸结合寡聚化结构域样受体蛋白3炎症小体在脑卒中后认知障碍中的研究进展

脑卒中后认知障碍(PSCI)是脑卒中患者常见的并发症,严重影响患者的生活质量。目前,PSCI在临床治疗中尚未发现有效的针对性治疗措施。大量研究证实核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎症小体的活化在PSCI中起关键作用,且对其进行的许多抑制性治疗显示出了改善认知障碍的功效。为此,本文总结了NLRP3炎症小体的活化和影响因素及其与PSCI的关系,发现在PSCI的细胞和动物模型中,针对NLRP3或其炎症小体成分的抑制措施可以减轻炎性反应和相应的病理特征,从而促进其认知功能的恢复,因此,靶向NLRP3炎症小体可能是PSCI治疗的新趋势。然而到目前为止,尽管许多药物和治疗措施已成功鉴定出能够抑制NLRP3炎症小体的活化,但其在临床中的治疗效果和安全性仍有待进一步验证。     

中国肥厚型心肌病患者血栓栓塞事件风险预测模型的构建研究

背景 血栓栓塞（TE）事件是肥厚型心肌病（HCM）的重要并发症。目前针对HCM患者TE事件的风险预测,仅国外学者构建了两个模型：HCM Risk-CVA及French HCM score,然而,现有研究发现HCM Risk-CVA模型对于中国HCM患者的临床价值较为有限。目的 本研究拟构建适合中国HCM患者的TE事件风险预测模型。方法本研究系回顾性队列研究,收集2010—2018年在四川大学华西医院就诊的537例HCM患者的病例资料。本研究通过电话随访或电子病历系统查询患者就诊记录,每6～12个月随访1次,直至出现终点事件或死亡或研究拟定的评估日期（2019-12-31）,终点事件定义为复合性TE事件。采用单因素和多因素Cox回归分析构建风险预测模型,并使用自助重抽样的方法进行内部验证。结果 537例患者中,24例患者有不同程度的数据缺失,最终纳入513例患者。中位随访时间为4.2(1.3,6.2)年,随访过程中42例（8.18%）发生TE事件,年发病率为2.10%[95%CI(1.47%,2.73%)]。根据多因素Cox回归模型构建TE事件风险预测模型,最终纳入年龄、既往TE事件、心...     

不同重复经颅磁刺激模式对脑卒中后上肢运动功能障碍干预效果的网状Meta分析

背景 上肢运动功能障碍是脑卒中后常见的后遗症之一,严重影响患者日常生活能力。重复经颅磁刺激（rTMS）作为常见的神经电生理技术对治疗脑卒中后上肢运动功能障碍有较好的疗效,但临床对不同rTMS干预模式的选择仍缺乏循证依据。目的 采用网状Meta分析方法比较rTMS的4种模式对脑卒中后上肢运动功能障碍患者的临床疗效。方法 计算机检索PubMed、Embase、Cochrane Library、Web of Science、中国生物医学文献数据库、中国知网、万方数据知识服务平台、维普网中有关rTMS治疗脑卒中后上肢运动功能障碍的随机对照试验,并通过追溯Meta分析的参考文献作为补充。检索时间均为建库至2022年2月,采用主题词和自由词结合方式进行。2名研究者进行文献筛选、资料提取及质量评价。采用RevMan 5.0软件和Stata 16.0软件进行统计学分析。结果 最终纳入17篇文献,790例患者,共涉及6种干预措施：高频rTMS(HF-rTMS)、低频rTMS(LF-rTMS)、间断性theta节律刺激（iTBS）、连续性theta节律刺激（cTBS）、假刺激、常规疗法。网状Meta分析结...     

基于贝叶斯多变量联合模型的体检人群脑卒中发病风险因素的纵向研究

背景 脑卒中是目前影响人类健康的主要公共卫生问题之一;健康体检纵向数据累积了大量的健康信息,由于缺失数据多、样本量小等诸多问题,导致其利用率低、重要信息未能得到充分挖掘,进而对常见慢性病的有效防控等工作带来一定困难。目的 基于贝叶斯多变量联合模型,探讨体检人群脑卒中发病风险因素,为慢性病风险因素分析提供新的方法。方法 本研究使用空军军医大学西京医院健康医学中心2008—2015年的体检资料。随访情况：以首次发生脑卒中为结局事件,发生结局事件立即停止随访;若未发生,到2015年体检信息收集完成后结束随访;体检间隔时间为1年。依据随访过程中是否发生脑卒中分为脑卒中组和非脑卒中组。纵向观察变量包括总胆固醇（TC）、三酰甘油（TG）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）、体质指数（BMI）和收缩压（SBP）。采用多因素Cox回归模型分析基线情况对脑卒中结局事件的影响;采用贝叶斯多变量联合模型,分析随访过程中TC、TG、LDL-C、HDL-C、BMI和SBP的纵向变化轨迹对脑卒中发病的影响。结果 本研究共纳入234例研究对象,1 581条纵向随访记录,平均随访时间为...     

Cardiovascular responses in paraplegic subjects during arm exercise

Summary The purpose of this study was to examine cardiovascular responses during arm exercise in paraplegics compared to a well-matched control group. A group of 11 male paraplegics (P) with complete spinal cord-lesions between T6 and T12 and 11 male control subjects (C), matched for physical activity, sport participation and age performed maximal arm-cranking exercise and submaximal exercise at 20%, 40% and 6070 of the maximal load for each individual. Cardiac output (Q _c) was determined by the CO₂ rebreathing method. Maximal oxygen uptake was significantly lower and maximal heart rate (f _c) was sigificantly higher in P compared to C. At the same oxygen uptakes no significant differences were observed inQ _c between P and C; however, stroke volume (SV) was significantly lower andf _c significantly higher in P than in C. The lower SV in P could be explained by an impaired redistribution of blood and, therefore, a reduced ventricular filling pressure, due to pooling of venous blood caused by inactivity of the skeletal muscle pump in the legs and lack of sympathetic vasoconstriction below the lesion. In conclusion, in P maximal performance appears to have been limited by a smaller active muscle mass and a lower SV despite the higher _c,max. During submaximal exercise, however, this lower SV was compensated for by a higherf _c and, thus at the same submaximal oxygen uptake,Q _c was similar to that in the control group.     

A Multi-Response Analysis of Learned Heart Rate Control

Thirty college students were classified on the basis of cold-pressor blood pressure responses and then randomly assigned to one of three treatment groups. One group merely tracked a visual analog display of their heart rate (tracking group). A second group attempted to increase and decrease its heart rate without the visual display (no-feedback group). A third group attempted to increase and decrease their heart rates with the aid of the visual heart rate display (feedback group). Results indicated that the heart rate changes produced by both the feedback and no-feedback groups were significantly greater than those observed in the tracking group. There was no significant difference between the former two groups. Results also demonstrated that high cold-pressor reactors were able to produce significantly larger heart rate changes than the low reactor subjects. A correlational analysis of physiological responses accompanying heart rate change suggested that the response topographies of the high and low cold-pressor reactors differed as well. Finally, results indicated no relationship between coronary-prone personality characteristics, as measured by the Jenkins Activity Scale, and either cold-pressor reactivity or heart rate control performance.     

Nitric oxide neurotoxicity

Derangements in glutamate neurotransmission have been implicated in several neurodegenerative disorders including, stroke, epilepsy, Huntington's disease, Alzheimer's disease, and amyotrophic lateral sclerosis (ALS). Activation of the N-methyl- -aspartate (NMDA) receptor subtype of glutamate receptors results in the influx of calcium which binds calmodulin and activates neuronal nitric oxide synthase (nNOS), to convent -arginine to citrulline and nitric oxide (NO). NO has many roles in the central nervous system as a messenger molecule, however, when generated in excess NO can be neurotoxic. Excess NO is in part responsible for glutamate neurotoxicity in primary neuronal cell culture and in animal models of stroke. It is likely that most of the neurotoxic actions of NO are mediated by peroxynitrite (ONOO−), the reaction product from NO and superoxide anion. In pathologic conditions, peroxynitrite and oxygen free radicals can be generated in excess of a cell antioxidant capacity resulting in severe damage to cellular constitutents including proteins, DNA and lipids. The inherent biochemical and physiological characteristis of the brain, including high lipid concentrations and energy requirements, make it particularly susceptible to free radical and oxidant mediated insult. Increasing evidence indicates that many neurologic disorders may have components of free radical and oxidative stress induced injury.     

Cardiorespiratory responses to exercise in acute hypoxia, hyperoxia and normoxia

There is a prevailing hypothesis that an acute change in the fraction of oxygen in inspired air (F _IO₂) has no effect on maximal cardiac output ( ), although maximal oxygen uptake ( ) and exercise performance do vary along with F _IO₂. We tested this hypothesis in six endurance athletes during progressive cycle ergometer exercise in conditions of hypoxia (F _IO₂=0.150), normoxia (F _IO₂=0.209) and hyperoxia (F _IO₂=0.320). As expected, decreased in hypoxia [mean (SD) 3.58 (0.45) l·min^–1, P<0.05] and increased in hyperoxia [5.17 (0.34) l·min^–1, P<0.05] in comparison with normoxia [4.55 (0.32) l·min^–1]. Similarly, maximal power ( ) decreased in hypoxia [334 (41) W, P<0.05] and tended to increase in hyperoxia [404 (58) W] in comparison with normoxia [383 (46) W]. Contrary to the hypothesis, was 25.99 (3.37) l·min^–1 in hypoxia (P<0.05 compared to normoxia and hyperoxia), 28.51 (2.36) l·min^–1 in normoxia and 30.13 (2.06) l·min^–1 in hyperoxia. Our results can be interpreted to indicate that (1) the reduction in in acute hypoxia is explained both by the narrowing of the arterio-venous oxygen difference and reduced , (2) reduced in acute hypoxia may be beneficial by preventing a further decrease in pulmonary and peripheral oxygen diffusion, and (3) reduced and in acute hypoxia may be the result rather than the cause of the reduced and skeletal muscle recruitment, thus supporting the existence of a central governor. Electronic Publication