Correlation between the Degree of Inflammation and Stress Indicators and Concurrent Cognitive Impairment in Patients with Severe Craniocerebral Injury

Abstract

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.