背景:颅脑损伤可引起炎症和氧化应激,并可能对认知功能产生永久影响。此外,随着时间的推移,炎性因子的过度表达和高水平的氧化应激将不利于颅脑损伤的恢复,进一步破坏神经元和其他细胞结构。在这项研究中,我们调查了重型颅脑损伤患者的炎症和应激指标的变化,并分析了与并发认知障碍的关联。
方法:选取龙游县人民医院2022年1月至2023年6月收治的82例重型颅脑损伤患者进行回顾性研究。记录并比较急性和慢性期的炎症因子水平和氧化应激程度。炎症指标包括白细胞介素-6(IL-6),白细胞介素-10(IL-10),肿瘤坏死因子-α(TNF-α)和C反应蛋白(CRP),氧化应激指标包括人类皮质醇(Cor),去甲肾上腺素(NE),超氧化物歧化酶(SOD)。使用简易精神状态检查(MMSE)评估患者的认知功能,并评估认知障碍的发生率。采用Spearman相关性分析炎症和氧化应激指标与MMSE评分的相关性;采用logistic回归分析影响患者并发认知障碍的相关因素;采用受试者工作特征(ROC)曲线检验炎症和氧化应激指标对患者并发认知障碍急性期和慢性期的预测价值。
结果:患者的IL-6、IL-10、TNF-α水平较高,CRP,Cor,NE,和较低水平的SOD,在急性期与慢性期相比(p<0.05)。急性期MMSE评分高于慢性期(p<0.05)。共50例并发认知障碍,认知障碍的发生率为60.98%。IL-6、IL-10、TNF-α、CRP,Cor,慢性阶段的NE与并发认知障碍呈正相关,SOD水平与并发认知障碍呈负相关(p<0.05)。单因素分析显示,年龄、IL-6、IL-10、TNF-α、CRP,Cor,认知障碍组的NE高于认知正常组,SOD水平低于正常认知组,初中和额叶损害的百分比高于认知正常组(p<0.05)。Logistic回归分析显示,初中,额叶损伤,较高水平的IL-6,IL-10,TNF-α,慢性期的CRP,慢性期SOD水平降低是影响患者并发认知障碍的相关因素。如ROC曲线所示,指标组合的曲线下面积(AUC)为0.949,敏感性为0.980,特异性为0.844.
结论:重型颅脑损伤患者认知障碍的发生率较高,以及炎症和氧化应激的水平,不利于恢复,在急性期患者中较高。识字水平较低的患者并发认知障碍的风险较高,额叶损伤,以及慢性阶段高水平的炎症因子和氧化应激;这些指标,因此,对患者的预后有显著的预测作用。
BACKGROUND: Craniocerebral injuries can cause inflammation and oxidative stress, and can have permanent effects on cognitive function. Moreover, over time, excessive expression of inflammatory factors and high levels of oxidative stress will be detrimental to recovery from craniocerebral injury and may exacerbate neurological damage, further damaging neurons and other cellular structures. In this study, we investigated changes in inflammation and stress indicators in patients with severe craniocerebral injuries, and analyzed associations with concurrent cognitive impairment.
METHODS: 82 patients with severe craniocerebral injuries admitted to Longyou County People\'s Hospital during January 2022-June 2023 were selected for retrospective study. Levels of inflammatory factors and the degree of oxidative stress were recorded and compared between the acute and chronic phases. Inflammatory measures included interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-α) and C-reactive protein (CRP), and oxidative stress indicators included human cortisol (Cor), norepinephrine (NE), and superoxide dismutase (SOD). The patients\' cognitive function was evaluated using the Mini-Mental State Examination (MMSE), and the incidence of cognitive impairment was assessed. Spearman\'s correlation was used to analyze associations between inflammatory and oxidative stress measures and MMSE scores; logistic regression was used to analyze the related factors affecting the patients\' concurrent cognitive impairment; and the receiver operating characteristic (ROC) curve was used to test the predictive value of inflammatory and oxidative stress measures on the patients\' concurrent cognitive impairment in the acute phase and the chronic phase.
RESULTS: Patients had higher levels of IL-6, IL-10, TNF-α, CRP, Cor, and NE, and lower levels of SOD, in the acute phase compared to the chronic phase (p < 0.05). MMSE scores were higher in the acute phase than in the chronic phase (p < 0.05). A total of 50 cases were complicated by cognitive impairment, and the incidence of cognitive impairment was 60.98%. The levels of IL-6, IL-10, TNF-α, CRP, Cor, and NE in the chronic phase were positively correlated with the concurrent cognitive impairment, and the level of SOD was negatively correlated with the concurrent cognitive impairment (p < 0.05). Single-factor analysis showed that age and levels of IL-6, IL-10, TNF-α, CRP, Cor, and NE were higher in the cognitively impaired group than in the cognitively normal group, SOD levels were lower than in the cognitively normal group, and percentages of below-secondary school and frontal lobe damage were higher than those in the cognitively normal group (p < 0.05). Logistic regression analysis showed that below-secondary school, frontal lobe injury, higher levels of IL-6, IL-10, TNF-α, and CRP in the chronic phase, and lower levels of SOD in the chronic phase were all relevant factors affecting the patients\' concurrent cognitive impairment. As shown by the ROC curve, the area under the curve (AUC) for the combination of indicators was 0.949, sensitivity was 0.980, and specificity was 0.844.
CONCLUSIONS: The incidence of cognitive impairment is higher in patients with severe craniocerebral injury, and the levels of inflammation and oxidative stress, which are not conducive to recovery, are higher in patients in the acute stage. The risk of concurrent cognitive impairment is higher in patients with a lower level of literacy, frontal lobe injury, and high levels of inflammatory factors and oxidative stress in the chronic stage; these indicators, therefore, have a significant predictive effect on the prognosis of the patients.