ABSTRACT
Background and purpose: Traumatic brain injury (TBI), especially the severe TBI are often followed by persistent cognitive sequalae, including decision-making difficulties, reduced neural processing speed and memory deficits. Diffuse axonal injury (DAI) is classified as one of the severe types of TBI. Part of DAI patients are marginalized from social life due to cognitive impairment, even if they are rated as favorable outcome. The purpose of this study was to elucidate the specific type and severity of cognitive impairment in DAI patients with favorable outcome. Methods: The neurocognition of 46 DAI patients with favorable outcome was evaluated by the Chinese version of the Montreal Cognitive Assessment Basic (MoCA-BC), and the differences in the domains of cognitive impairment caused by different grades of DAI were analyzed after data conversion of scores of nine cognitive domains of MoCA-BC by Pearson correlation analysis. Results: Among the 46 DAI patients with favorable outcome, eight had normal cognitive function (MoCA-BC ≥ 26), and 38 had cognitive impairment (MoCA-BC < 26). The MoCA-BC scores were positively correlated with pupillary light reflex (r = 0.361, p = 0.014), admission Glasgow Coma Scale (GCS) (r = 0.402, p = 0.006), and years of education (r = 0.581, p < 0.001). Return of consciousness (r = -0.753, p < 0.001), Marshall CT (r = -0.328, p = 0.026), age (r = -0.654, p < 0.001), and DAI grade (r = -0.403, p = 0.006) were found to be negatively correlated with the MoCA-BC scores. In patients with DAI grade 1, the actually deducted scores (Ads) of memory (r = 0.838, p < 0.001), abstraction (r = 0.843, p < 0.001), and calculation (r = 0.782, p < 0.001) were most related to the Ads of MoCA-BC. The Ads of nine cognitive domains and MoCA-BC were all proved to be correlated, among patients with DAI grade 2. However, In the DAI grade 3 patients, the highest correlation with the Ads of MoCA-BC were the Ads of memory (r = 0.904, p < 0.001), calculation (r = 0.799, p = 0.006), orientation (r = 0.801, p = 0.005), and executive function (r = 0.869, p = 0.001). Conclusion: DAI patients with favorable outcome may still be plagued by cognitive impairment, and different grades of DAI cause different domains of cognitive impairment.
ABSTRACT
Background: Moderate to severe traumatic brain injury (TBI) is frequently accompanied by diffuse axonal injury (DAI). Considering the low sensitivity of computed tomography (CT) examination for microbleeds and axonal damage, identification of DAI is difficult using conventional diagnostic methods in the acute phase. Neuron-specific enolase (NSE) has been demonstrated to be increased in serum following various types of TBI and is already clinically/commercially available. We conjecture that serum NSE level to admission GCS score ratio (NGR) may be a useful indicator for the early diagnosis of DAI. Methods: This study included 115 patients with moderate-to-severe TBI who underwent NSE measurements within 6 h after injury and brain magnetic resonance imaging (MRI) within 30 days. The positive and negative DAI groups were divided according to MRI findings. Results: Among the 115 patients, 49 (42.6%) were classified into the DAI group and 66 (57.4%) patients into the non-DAI group by clinical MRI. The NGR of patients without DAI was found to be significantly lower than those of patients with DAI (p < 0.0001). NGR presented the largest Pearson r value (r = 0.755, 95% CI 0.664-0.824, p < 0.0001) and high diagnostic accuracy for DAI [area under the curve (AUC) = 0.9493; sensitivity, 90.91%; and specificity, 85.71%]. Patients with TBI presenting with higher NGR were more likely to suffer an unfavorable neurological outcome [6-month extended Glasgow Outcome Scale (GOSE) 1-4]. Conclusions: The NGR on admission could serve as an independent predictor of DAI with moderate-to-severe TBI.
ABSTRACT
Impairments of tight junctions are implicated in the course of various age-related neurodegenerative disorders. Chronic injection of D-galactose can cause a progressive deterioration in learning and memory capacity and serve as an animal model of aging. To investigate the involvement of tight junctions in this model, oxidative stress biomarkers, expression and ultrastructure of tight junctions, and the permeability of blood-brain barrier were examined in the hippocampus of the mice, which received an injection of D-galactose for 6 weeks. D-Galactose-injected mice showed impaired antioxidant systems, decreased levels of tight junction proteins, and ultrastructural pathological changes of tight junctions, accompanied by increased blood-brain barrier permeability in the hippocampus. These results show that impairments in tight junctions are involved in D-galactose-induced brain aging.
