Cerebral Complications of Snakebite Envenoming: Case Studies

There are an estimated 5.4 million snakebite cases every year. People with snakebite envenoming suffer from severe complications, or even death. Although some review articles cover several topics of snakebite envenoming, a review of the cases regarding cerebral complications, especially rare syndromes, is lacking. Here, we overview 35 cases of snakebite by front-fanged snakes, including Bothrops, Daboia, Cerastes, Deinagkistrodon, Trimeresurus, and Crotalus in the Viperidae family; Bungarus and Naja in the Elapidae family, and Homoroselaps (rare cases) in the Lamprophiidae family. We also review three rare cases of snakebite by rear-fanged snakes, including Oxybelis and Leptodeira in the Colubridae family. In the cases of viper bites, most patients (17/24) were diagnosed with ischemic stroke and intracranial hemorrhage, leading to six deaths. We then discuss the potential underlying molecular mechanisms that cause these complications. In cases of elapid bites, neural, cardiac, and ophthalmic disorders are the main complications. Due to the small amount of venom injection and the inability to deep bite, all the rear-fanged snakebites did not develop any severe complications. To date, antivenom (AV) is the most effective therapy for snakebite envenoming. In the six cases of viper and elapid bites that did not receive AV, three cases (two by viper and one by elapid) resulted in death. This indicates that AV treatment is the key to survival after a venomous snakebite. Lastly, we also discuss several studies of therapeutic agents against snakebite-envenoming-induced complications, which could be potential adjuvants along with AV treatment. This article organizes the diagnosis of hemotoxic and neurotoxic envenoming, which may help ER doctors determine the treatment for unidentified snakebite.     

Chronic hyperammonemia alters the circadian rhythms of corticosteroid hormone levels and of motor activity in rats

Patients with liver cirrhosis may present hepatic encephalopathy with a wide range of neurological disturbances and alterations in sleep quality and in the sleep‐wake circadian rhythm. Hyperammonemia is a main contributor to the neurological alterations in hepatic encephalopathy. We have assessed, in an animal model of chronic hyperammonemia without liver failure, the effects of hyperammonemia per se on the circadian rhythms of motor activity, temperature, and plasma levels of adrenal corticosteroid hormones. Chronic hyperammonemia alters the circadian rhythms of locomotor activity and of cortisol and corticosterone levels in blood. Different types of motor activity are affected differentially. Hyperammonemia significantly alters the rhythm of spontaneous ambulatory activity, reducing strongly ambulatory counts and slightly average velocity during the night (the active phase) but not during the day, resulting in altered circadian rhythms. In contrast, hyperammonemia did not affect wheel running at all, indicating that it affects spontaneous but not voluntary activity. Vertical activity was affected only very slightly, indicating that hyperammonemia does not induce anxiety. Hyperammonemia abolished completely the circadian rhythm of corticosteroid hormones in plasma, completely eliminating the peaks of cortisol and corticosterone present in control rats at the start of the dark period. The data reported show that chronic hyperammonemia, similar to that present in patients with liver cirrhosis, alters the circadian rhythms of corticosteroid hormones and of motor activity. This suggests that hyperammonemia would be a relevant contributor to the alterations in corticosteroid hormones and in circadian rhythms in patients with liver cirrhosis. © 2009 Wiley‐Liss, Inc.     

白芍总甙对局灶性脑缺血大鼠脑组织炎症信号表达的影响

目的观察白芍总甙对局灶性脑缺血(Focal Cerebral ischemic,FCI)大鼠脑组织Toll样受体4(TLR4)基因表达的作用。方法参照longa等方法制成大鼠局灶性大脑中动脉梗死(MCAO)模型,将80只SD雄性大鼠随机分为假手术组,溶剂组,白芍总甙低、高两个剂量组,采用RT-PCR法检测缺血灶周围脑组织TLR4基因表达水平。结果生理盐水组TLR4基因相对表达均明显高于假手术组(P<0.01);白芍总甙中高剂量组TLR4相对表达量明显低于生理盐水组(P<0.01)。结论生理盐水组大鼠缺血灶周围脑组织TLR4基因高表达,白芍总甙对TLR4表达有抑制作用,这可能是其抗炎作用的机理之一。     

急性一氧化碳中毒后迟发性脑病与自由基关系的初步研究

测定了３１例急性一氧化碳中毒后迟发性脑病患者血清过氧化脂质（ＬＰＯ）、水溶性脂质过氧化物（ＷＳＦＳ）、谷胱甘肽过氧化物酶（ＧＰＸ）、维生素Ｅ（ＶＥ）的含量，并与健康者作了比较。结果表明，患者血清中ＬＰＯ、ＷＳＦＳ含量明显增高，ＧＰＸ、ＶＥ含量明显降低，与对照组比较有显著性差异。患者组治疗１个月后复查，结果上述指标均有不同程度改变，且与病情变化基本一致。提示自由基可能在本病发病中起重要作用。     

急性一氧化碳中毒迟发性脑病的MRI诊断

目的 探讨急性一氧化碳中毒迟发性脑病的MRI表现，提高对该病的正确诊断率。资料与方法 总结和分析临床证实的19例急性一氧化碳中毒迟发性脑病的MRI表现。结果 (1)脑白质异常信号7例，主要分布于侧脑室旁的脑白质及半卵圆中心，为大片状长T1、长T2信号，呈对称分布。(2)苍白球斑点状异常信号4例，其中3例为双侧苍白球对称性长T1、长T2信号，1例为右侧苍白球短T1、长T2信号并左侧黑质点状长T1、长L信号。(3)侧脑室旁脑白质及半卵圆中心对称长T1、长T2信号并基底节异常信号8例。有7例并双侧苍白球异常信号，3例为长T1、长T2信号，4例为短T1、长T2信号；1例并右侧内囊及左侧尾状核头部短T1、长T2信号。结论 MRI是诊断急性一氧化碳中毒迟发性脑病的最佳影像学检查方法。     

缺血性脑血管病304例血管造影分析

目的 分析缺血性脑血管病(ICVD)患者脑供血动脉狭窄或闭塞发生的特点.方法 回顾性分析304例ICVD患者的DSA资料,其中短暂性脑缺血(11A)188例,脑梗死116例,明确有无脑供血动脉的狭窄、狭窄的位置,判断责任血管.测量责任血管狭窄段长度及程度.结果 304例ICVD患者中发现脑供血动脉狭窄或闭塞227例(74.7%),可判断责任血管193例(85.0%),其中单纯颅外血管病变104例(53.9%),单纯颅内血管病变70例(36.3%),颅内外串联病变19例(9.8%),TLA组的后循环颅外血管病变的发生率高于脑梗死组,脑梗死组的前循环颅内血管病变的发生率高于TIA组.两组责任血管狭窄的长度及严重程度均无明显差异(P＞0.05).结论 重症缺血性脑血管病患者脑供血动脉狭窄或闭塞更多见,但责任血管狭窄的严重程度和长度与症状严重程度无关.     

脐动脉血pH值评价新生儿窒息的临床应用价值

目的探讨脐动脉血pH值评价新生儿窒息及预测窒息并发症的临床意义。方法抽取2006年1月—2008年4月在我院分娩的健康产妇552例。监测其新生儿脐动脉血pH值,分析脐动脉血pH值与生后1 min Apgar评分的关系,分别对脐动脉血pH值及1 min Apgar评分对于预测新生儿窒息并发症进行真实性的评价。结果1 min Apgar评分与脐动脉血pH值相关(χ2=278.13,P<0.05)。脐动脉血pH值对于预测窒息并发症较Apgar评分有更高的敏感度及特异度。pH值异常发生比例与HIE程度有关,随HIE程度的提高而增加(χ2=4.437,P<0.05)。结论脐动脉血pH值能客观评价新生儿出生时的状况,对监测新生儿预后、早期采取有效措施防治窒息并发症有指导意义。     

新生儿缺氧缺血性脑病43例临床与预后分析

分析新生儿缺氧缺血性脑病（ＨＩＥ）４３例。有宫内窘迫史者占５８１％,出生重度窒息占８１４％。ＨＩＥ轻度１０例,中度２６例,重度７例。合并心肌损害达４１７％。治愈好转率为８１３％。病死率７０％。随访２４例,轻度ＨＩＥ预后好,中度有明显后遗症者为６７％,重度预后不良。认为加强围生期保健,提高产科质量,进行新法复苏及复苏后处理是降低ＨＩＥ发病率的关键。诊治中应重视心肌损害。使用胞二磷胆碱等脑细胞代谢激活剂辅治ＨＩＥ效果肯定。对于预后,强调早期治疗,早期评分、早期随访、早期干预是改善重度ＨＩＥ预后的几个重要环节。