Influence of mouse nerve growth factor combined with hyperbaric oxygen on serum cytokines and cognitive function in patients with delayed encephalopathy after carbon monoxide poisoning

Objective:To study the influence of mouse nerve growth factor (mNGF) combined with hyperbaric oxygen on serum cytokines and cognitive function in patients with delayed encephalopathy after carbon monoxide poisoning (DEACMP).Methods: 218 patients with DEACMP who were treated in our hospital between June 2012 and September 2016 were chosen as research subjects and retrospectively divided into the control group (n=100) who underwent hyperbaric oxygen treatment and the observation group (n=118) who underwent mouse nerve growth factor combined with hyperbaric oxygen treatment. Serum contents of nerve injury indexes and inflammatory mediators were compared between two groups of patients and cognitive function was assessed.Results:Before treatment, differences in serum levels of nerve injury indexes and inflammatory mediators, total MMSE score and each dimension score were not statistically significant between two groups of patients. After treatment, serum contents of nerve injury indexes creatine kinase-BB (CK-BB), neuron-specific enolase (NSE), S-100β protein (S-100β) and lactate (Lac) in observation group were lower than those in control group;serum contents of inflammatory mediators interleukin-6 (IL-6), interleukin-10 (IL-10), interleukin-18 (IL-18), hypersensitive C-reactive protein (hs-CRP) and tumor necrosis factor (TNF-α) were lower than those in control group;total MMSE score and each dimension score were higher than those of control group.Conclusion:mNGF combined with hyperbaric oxygen treatment of DEACMP is helpful to reduce the nerve injury and systemic inflammatory response, and improve the cognitive function.

Massive subdural hematoma misdiagnosed as delayed encephalopathy of carbon monoxide poisoning: a case report and literature review

Subdural hematoma is often secondary to brain trauma and other diseases.The onset is hidden and the condition is critical.Timely detection and early treatment are particularly important.The patient denied a history of trauma,but had a history of consciousness loss after charcoal burning.The clinical symptoms were progressive cognitive impairment.The initial diagnosis was delayed encephalopathy caused by carbon monoxide poisoning.However,computed tomography(CT)scan of the brain showed a large area of subdural hematoma on the left side and the formation of a cerebral hernia,which was life-threatening.The patienfs symptoms gradually improved after an emergency operation.

Multimodality evoked potentials in patients with delayed encephalopathy after acute carbon monoxide poisoning

Objective： To evaluate the diagnostic and prognostic values in patients with delayed encephalopathy after acute carbon monoxide poisoning. Methods： The tibial nerve somatosensory evoked potentials （SEPs）, vision evoked potentials （VEPs）, and brain stem audition evoked potentials（BAEPs） were performed in 32 healthy adults and 43 patients with delayed encephalopathy after acute carbon monoxide poisoning. Results： This paper indicated abnormalities of tibial nerve SEPs in 31 patients （31/43, 72.1%）, VEPs in 17 patients （17/28, 60.7%）, and BAEPs in 14, patients （14/43, 32.6%）. These results showed that the greatest diagnostic value was SEPs, followed by VEPs and, BAEPs with the lowest sensitivity. Conclusion： Multimodality evoked potentials （EPs） can be used for evaluating the diagnostic and prognostic values in cases of delayed encephalopathy after acute carbon monoxide poisoning.

Brainstem auditory evoked potentials in patients with delayed encephalopathy after acute carbon monoxide poisoning

Objective:To evaluate the changes of brainstem auditory evoked potential (BAEP) in patients with delayed encephalopathy after acute carbon monoxide poisoning. Methods: BAEPs were performed in 32 controls and 40 patients. Wave Ⅰ , Ⅱ , Ⅲ ,Ⅳ, Ⅴ latencies and Ⅰ-Ⅲ , Ⅲ-Ⅴ , Ⅰ-Ⅴ interpeak latencies were measured, respectively. Results: Abnormalities of BAEPs in 13 patients (13/40, 32 ％). Among the13 abnormal BAEPs, 3 displayed prolongation of latency to waves in one side, no potential in another side; 5 displayed a similar abnormality which was bilateral prolongation of latency to waves ;and another 5 displayed unilateral latency delay. Compared wave Ⅰ , Ⅱ , Ⅲ , Ⅳ, Ⅴ latencies and Ⅰ-Ⅲ , Ⅲ-Ⅴ , Ⅰ-Ⅴ interpeak latencies in the patients and the controls, there were no significant differences (P＞0.05). Conclusion: BAEPs can be used for evaluating the diagnostic and prognostic values in the cases of delayed encephalopathy after acute carbon monoxide poisoning.

Early Biomarkers in 1H Nuclear Magnetic Resonance Spectroscopy of Striatal Pathological Mechanisms after Acute Carbon Monoxide Poisoning in Rats

Objective In vivo Proton Magnetic Resonance Spectroscopy （1H-MRS） can be used to evaluate the levels of specific neurochemical biomarkers of pathological mechanisms in the brain. Methods We conducted T2-Weighted Magnetic Resonance Imaging （MRI） and 1H-MRS with a 3.0-Tesla animal MRI system to investigate the early microstructural and metabolic profiles in vivo in the striatum of rats following carbon monoxide （CO） poisoning. Results Compared to baseline, we found significant cortical surface deformation, cerebral edema changes, which were indicated by the unclear gray/white matter border, and lateral ventricular volume changes in the brain. A significant reduction in the metabolite to total creatine （Cr） ratios of N-acetylaspartate （NAA） was observed as early as 1 h after the last CO administration, while the lactate （Lac） levels increased marginally. Both the Lac/Cr and NAA/Cr ratios leveled off at 6 h and showed no subsequent significant changes. In addition, compared to the control, the choline （Cho）/Cr ratio was slightly reduced in the early stages and significantly increased after 6 h. In addition, a pathological examination revealed mild cerebral edema on cessation of the insult and more severe cerebral injury after additional CO poisoning. Conclusion The present study demonstrated that 1H-MRS of the brain identified early metabolic changes after CO poisoning. Notably, the relationship between the increased Cho/Cr ratio in the striatum and delayed neuropsychologic sequelae requires further research.

Assessment of rehabilitation treatment for patients with acute poisoning-induced toxic encephalopathy

BACKGROUND:Poisoned patients often suffer damage to multiple systems,and those experiencing central nervous system disorders present more severe conditions,prolonged hospital stays,and increased mortality rates.We aimed to assess the efficacy of rehabilitation interventions for patients with toxic encephalopathy.METHODS:This retrospective,observational,comparative cohort study was performed at the teaching hospital affiliated of Nanjing Medical University,from October 2020 to December 2022.Patients who met the diagnostic criteria for toxic encephalopathy and exclusion criteria were included,and patients were divided into three subgroups according to Glasgow Coma Scale(GCS).Demographic and clinical characteristics were collected.The effect of the rehabilitation intervention on patients were assessed in the improvement of consciousness status(Glasgow Coma Scale[GCS]score),muscle strength and movement and swallowing function(Fugl-Meyer Assessment[FMA]scale,Water Swallow Test[WST],and Standardized Swallowing Assessment[SSA]).Subgroup analysis was based on different toxic species.RESULTS:Out of the 464 patients with toxic encephalopathy,184 cases received rehabilitation treatments.For the severe toxic encephalopathy patients,patients without rehabilitation intervention have a 2.21 times higher risk of death compared to patients with rehabilitation intervention(Hazard ratio[HR]=2.21).Subgroup analysis revealed that rehabilitation intervention significantly increased the survival rate of patients with pesticide poisoning(P=0.02),while no significant improvement was observed in patients with drug/biological agent poisoning(P=0.44).After rehabilitation intervention,significant improvement in GCS and FMA were observed in severe patients with toxic encephalopathy(P<0.01).CONCLUSION:Active rehabilitation intervention for patients exposed to poisons that can potentially cause toxic encephalopathy may improve the prognosis and reduce the mortality rate in clinical practice.

Acute carbon monoxide poisoning and delayed neurological sequelae: a potential neuroprotection bundle therapy

Currently, there is no known optimal therapy for carbon monoxide （CO） poisoning and CO-associated delayed neu- rological sequelae. Hyperbaric oxygen therapy （HBOT） is a well-known treatment method, but its use for CO poison- ing patients is controversial to use due to lack of evidences regarding its efficacy. Thus, it is unlikely that HBOT alone will be accepted as the standard treatment method. In this article, current and potential treatment methods of CO poi- soning are presented as well as the tentative multi-factorial pathophysiology. A series of treatments are suggested for use as a bundle therapy, with targeted temperature management as the base treatment method. Such a therapy holds a great potential, especially for the cases where HBOT is not readily available. We suggest further investigations for elucidating the effects of these suggested treatments and their roles in terms of the complex pathophysiology of CO poisoning. Future ac- ceptance of this therapy based on the improved scientific and clinical knowledge may result in injury prevention and mini- mization of the signs and the symptoms in CO poisoning.

Hippocampus hypoxia-inducible factor-1 alpha and heme oxygenase-1 expression in the delayed encephalopathy after acute carbon monoxide poisoning rat model

Objective To research the expression of hypoxia-inducible factor-1 alpha(HIF-1α)and heme oxygenase-1(HO-1)in hippocampus of rats with delayed encephalopathy after acute carbon monoxide poisoning(DEACMP)and its functions.Methods One hundred and fiftysix rats were selected and randomly divided into

ADC值的变化对急性CO中毒迟发性脑病的预测价值

目的利用MR扩散加权成像监测CO中毒家兔模型急性期脑组织ADC值的变化并与病理对照,探讨MR扩散加权成像对CO中毒急性期诊断的价值并尝试寻找一种能预测CO中毒迟发性脑病的指标。方法通过静吸法建立家兔CO中毒模型15只,成功13只。行磁共振功能成像(本文主要探讨MR扩散加权成像)动态观察家兔中毒后1 h、第3天、第5天、第7天的脑部损伤情况,动态测量兔脑皮层的ADC值,并结合病理结果分别与中毒前ADC值相对照。与此同时,连续观察染毒家兔临床表现60 d,并根据临床表现不同分为两组,即出现迟发性脑病组和未出现迟发性脑病组。结果所有染毒成功家兔在染毒后1 h兔脑皮层均出现ADC值不同程度下降,平均ADC值与染毒前对照差别有显著性(P<0.05),部分出现了异常信号;未出现迟发性脑病的家兔组各时间点脑皮层ADC值与染毒前对照差异均无显著性意义(P>0.05);出现迟发性脑病的家兔组染毒后1 h脑皮层ADC值与染毒前对照差异有显著性(P<0.05)。病理表现与影像学表现一致。结论ADC值对评价急性CO中毒的程度具有重要价值,并且可以初步预测CO中毒迟发性脑病发生的可能性。

Correlations between delayed fluorescence of chlorophyll, metabolism and yield of plants. I. Influence of fertilizers on correlations

The increase of the potash fertilizer dose in-duced a raise in efficiency influence of the ni-trogen fertilizer, optimisation of phosphorous fertilizer effect, enhancement of leaf protein production, expansion of assimilating surface and yield growth. In the period of yield forma-tion, the parameters of delayed fluorescence of chlorophyll (DF) of leaf wholly corresponded with key factors that had a dramatic influence on the effectiveness of yield formation. The maximum level of DF amplitude mostly de-pended on the activity of nitrogen metabolism and presumably on active PSII concentration changes per square unit. Half-decay time of this amplitude was predominantly identified by the level of carbohydrate metabolism in the overall plant system, including the quantity of its products and, therefore, mostly by correspon-dence with yield. This is a biological base trig-gering the use of DF parameters for system analyses of plant production process.

急性CO中毒后迟发性脑病的相关因素及P_(300)的研究

目的 探讨急性一氧化碳 (CO)中毒后迟发性脑病 (DEACMP)的相关因素及P3 0 0 对其病情判定和预后的意义。方法 对 4 4例DEACMP患者与 4 2例未发生迟发性脑病的急性CO中毒 (ACMP)患者在CO接触时间、昏迷时间等 13个方面进行比较 ,并行P3 0 0 检测 ,且与DEACMP组发生CO中毒初期清醒后所测P3 0 0(DEACMP0组 )及 4 4名正常人的P3 0 0 (NC组 )进行比较。结果 DEACMP在CO接触时间、昏迷时间、高压氧治疗时间、年龄、合并症等方面与ACMP组比较有极显著差异 (P <0 .0 1) ,在扩血管药治疗、心脑血管病及呼吸系统疾病史、吸烟、职业方面亦有显著差异 (P <0 .0 5 )。DEACMP组较DEACMP0组P3 0 0 潜伏期明显延长 ,波幅明显下降 (P <0 .0 1) ,DEACMP0组较NC组亦有类似改变。结论 长时间接触CO、长时间昏迷、高压氧治疗时间较短、扩血管药治疗时间短、年龄较大、有合并症、患心脑血管病及呼吸系统疾病、吸烟、脑力劳动与发生DEACMP相关。急性CO中毒患者的P3 0 0 潜伏期越长、波幅越低、其认知功能越差 ,发生DEACMP的可能性越大。P3 0 0 对DEACMP的发生。

46例CO中毒脑病病例脑部MRI影像特征及ADC值分析

目的探讨急性一氧化碳中毒(ACOP)脑病患者脑部MRI影像特征及弥散加权成像表观弥散系数(ADC)值分析的临床价值。方法回顾性分析46例急性CO中毒迟发性脑病(DEACMP)患者(观察组)及30例健康志愿者(对照组)脑部MRI影像及临床资料,分析其影像特征。对比两组受试者皮质区、半卵圆中心区、侧脑室周围白质区、苍白球区等相同部位的ADC平均值差异。结果 46例观察组受试者中15例(32.6%)MRI影像表现正常(无重度ACOP者,轻度14例、中度1例);剩余31例受试者头颅MRI影像可见异常信号,其中大脑皮质区受累2例,双侧顶叶皮质区可见T1WI对称性低信号、T2WI及DWI呈对称性高信号;双侧苍白球区异常信号者19例,表现为对称性长T1、长T2信号,呈现典型的"熊猫眼"特征;双侧脑白质区异常信号者10例,MRI图像可见对称分布的斑片状异常信号影,T1WI呈稍低信号,T2WI呈稍高信号,脑沟及脑裂均未见异常。观察组皮质区、半卵圆中心区、侧脑室周围白质区、苍白球区等部位ADC平均值均显著低于对照组,差异具有统计学意义(P<0.05)。结论 MRI在DEACMP的临床诊断中具有明显的影像特征,联合ADC值评估可有效提高诊断准确性,为后续诊疗工作的顺利开展提供条件。

依达拉奉联合高压氧对急性CO中毒迟发性脑病小鼠学习记忆能力的影响

目的探讨依达拉奉联合高压氧对急性CO中毒迟发性脑病小鼠学习记忆能力的影响。方法通过腹腔注射CO建立急性CO中毒迟发性脑病小鼠模型。小鼠随机分成6组,从染毒后第3周开始各组使用不同方法连续治疗14 d,治疗结束后使用Morris水迷宫检测学习记忆能力,以平均潜伏期及空间探索次数来比较各组学习记忆的差异。结果 DEACMP组小鼠平均潜伏期高于对照组(P<0.05),空间探索成绩低于对照组(P<0.05);染毒后小鼠除生理盐水组其余各组平均潜伏期均低于DEACMP组(P<0.05),空间探索成绩均高于DEACMP组(P<0.05);联合治疗组平均潜伏期低于高压氧组及依达拉奉组(P<0.05),空间探索成绩高于高压氧组及依达拉奉组(P<0.05)。结论依达拉奉联合高压氧可以有效改善急性CO中毒迟发性脑病小鼠空间学习记忆能力,效果优于单纯高压氧治疗。

急性CO中毒迟发性脑病的MRI表现

目的:探讨急性CO中毒迟发性脑病(DEACMP)的MRI特征。方法:回顾性分析21例急性CO中毒迟发性脑病患者的MRI和临床资料。结果:急性CO中毒迟发性脑病MRI表现可分为3种:①神经核团受累:21例,典型表现为双侧苍白球对称性的长T1、长T2信号;②脑白质受累:11例,表现为双侧大脑半球白质对称云絮状长T1、长T2信号,胼胝体常受累;③皮层受累:6例,表现为双侧大脑半球皮层对称性弥漫长T1、长T2信号。结论:急性CO中毒迟发性脑病MRI表现有一定特征性,MRI对急性CO中毒迟发性脑病的诊断、鉴别诊断、判断预后具有重要价值。

氧应激对急性CO中毒迟发性脑病的作用研究

目的 探讨氧应激对CO中毒家兔血液流变学的影响及在CO中毒迟发性脑病中的可能作用。方法 家兔CO染毒后 ,自耳缘静脉注射 0 3 %双氧水溶液进行干预 ,每日 3次 ,共进行 2d。同时检测染毒动物 2 1d内血液粘度、红细胞变形性和红细胞压积的变化 ,并作血浆SOD、MDA含量测定。结果 动物CO染毒后血粘度、红细胞压积等迅速下降 ,后持续异常增高 ,给氧组动物在 3～ 14天内增高更为明显 ,差异有显著性 ;染毒后 1～ 3天内动物血浆SOD活力降低 ,给氧组家兔降低更为明显 ;染毒后家兔血浆MDA含量明显增高 ,给氧后增高更为显著 ,但两组间差异无显著性。结论 CO中毒后反复进行给氧干预可对机体血液流变学产生不利影响 ,并可加剧过氧化反应 。

低强度He-Ne激光血管内照射辅助治疗急性CO中毒后迟发性脑病

目的 观察低强度He Ne激光血管内照射 (ILLLI)治疗CO中毒后迟发性脑病 (DEACMP)的疗效。方法 1 84例DEACMP患者随机分为常规组 (常规药物及高压氧治疗 ,98例 )及ILLLI组 (常规治疗 +ILLLI治疗 ,86例 ) ,观察患者治疗前后的临床表现、智能、脑电图 (EEG)情况。结果 两组患者治疗后临床表现、智能、EEG较治疗前均有显著改善 ,ILLLI组较常规组改善更显著。结论 ILLLI对DEACMP的治疗有辅助作用。

Cox比例风险模型分析对急性一氧化碳中毒迟发性脑病的早期预测评价

目的对早期预测急性一氧化碳中毒迟发性脑病的相关因素进行评价。方法回顾性研究分析143例急性一氧化碳中毒患者,在患者入院后统计年龄、性别、基础病、并发症、中毒昏迷时间、高压氧治疗时间、恢复期精神刺激、白细胞计数、高敏C反应蛋白9项相关因素,应用Cox比例风险模型检验各因素与急性一氧化碳中毒迟发性脑病的关系。结果基础病、中毒昏迷时间、高压氧治疗时间、恢复期精神刺激和高敏C反应蛋白5个因素对预测急性一氧化碳中毒迟发性脑病的发生有统计学意义,而年龄、性别、并发症、白细胞计数和血清肌酸激酶同工酶(CK-MB)对急性一氧化碳中毒迟发性脑病的预测无统计学意义。结论应用Cox比例风险模型能够分析急性一氧化碳中毒迟发性脑病的独立预测因素,基础病、中毒昏迷时间、高压氧治疗时间、恢复期精神刺激及高敏C反应蛋白是预测急性一氧化碳中毒迟发性脑病的主要因素。

Morris水迷宫在筛选急性CO中毒迟发性脑病模型中的应用

目的探索Morris水迷宫的定位航行实验在连续筛选急性CO中毒迟发性脑病(DEACMP)模型中的应用价值。方法选择成年雄性SD大鼠,经过Morris水迷宫的定位航行试验训练,剔除60 s以上找到平台的SD大鼠,筛选合格SD大鼠108只,随机分为DEACMP组(腹腔注射纯品CO气体)、空气组(腹腔注射空气)、空白组(不进行任何预处理),每组36只。将三组各分成6个亚组(造模前、造模后第1天、第7天、第14天、第21天、第28天),每个亚组6只。从首次造模后2 h开始至24 h监测动脉碳氧血红蛋白(HbCO)浓度,在6个筛选时点上行Morris水迷宫定位航行试验,检测DEACMP大鼠认知功能,筛选出DEACMP模型,同时制备大鼠脑组织石蜡切片,观察海马CA3区变性坏死的神经元。结果(1)DEACMP组的平均潜伏期与空白组、空气组比较,在造模前、造模后第1天、第7天差异均无统计学意义(P均>0.05),而在第14天、第21天、第28天均长于空白组、空气组(P均<0.05)。(2)HE染色观察海马CA3区神经元变性坏死,将这种变性坏死神经元定为阳性细胞。DEACMP组的阳性细胞计数与空白组、空气组比较,在造模前、造模后第1天、第7天差异均无统计学意义(P均>0.05),而在第14天、第21天、第28天多于空白组、空气组(P均<0.05)。(3)Pearson相关性分析,DEACMP组染毒前后不同时间段的平均潜伏期与阳性细胞数之间呈正相关(r=0.915,P<0.001)。结论Morris水迷宫的定位航行实验是一种简易的检测DEACMP大鼠认知功能的可靠方法。

急性 CO 中毒后迟发性脑病的临床研究

目的：探讨急性ＣＯ中毒后迟发性脑病（ＤＥＡＣＭＰ）的发病机理、诊断和治疗方法。方法：对本病患者的多项免疫和生化指标进行检测，观察患者的脑电图（ＥＥＧ）、脑电地形图（ＢＥＡＭ）、诱发电位（ＶＰ）和脑ＣＴ改变及高压氧（ＨＰＯ）和紫外线照射充氧自血回输疗法（ＵＢＩＯ）对本病的疗效。结果：本病患者的多项免疫和生化指标有不同程度改变，ＥＥＧ、ＢＥＡＭ、ＶＰ和ＣＴ检查有不同程度异常，两种疗法的近期显效率均明显高于对照组。结论：免疫功能紊乱、神经递质和自由基代谢异常在ＤＥＡＣＭＰ的发生和病理发展过程中起重要作用，ＥＥＧ、ＢＥＡＭ、ＶＰ和ＣＴ检查对诊断和预后判断均有一定价值，ＨＰＯ和ＵＢＩＯ治疗疗效显著。

NF-κB/nNOS信号通路在小鼠急性CO中毒迟发性脑病发生中的作用

目的:分析NF-κB/n NOS信号通路在急性CO中毒迟发性脑病(DEACMP)中的作用。方法:将昆明雄性小鼠随机分为空气组与CO中毒组,其中空气组和CO中毒组又分别分为1、3、7、14和21 d亚组。CO中毒组小鼠首次腹腔注射99. 9%CO气体100 ml/kg,随后3次按首次剂量的半量(50 ml/kg)作追加注射,间隔为4 h,空气组以同样的方法注射等量空气,立即观察其精神状态和行为变化;并通过改良双波长碳氧血红蛋白(COHB)定量法动态监测小鼠血中COHB浓度;使用旷场实验和筑巢实验进行行为学监测;并用ELSIA法测定脑组织内髓鞘碱性蛋白(MBP)含量,筛选出DEACMP模型小鼠。用ELISA法分别检测脑组织中NF-κB和n NOS蛋白,用紫外分光光度计法测定脑组织中一氧化氮(NO)含量。结果:与空气组相比,CO中毒组旷场实验垂直站立次数和进入旷场中心次数均明显减少(P <0. 01),CO中毒组筑巢得分明显下降(P <0. 05),CO中毒组小鼠MBP、NF-κB、n NOS蛋白水平及NO含量于第3、7、14和21 d均明显增高(P <0. 01)。结论:NF-κB/n NOS信号通路可能参与了DEACMP的发生和发展。