Traumatic brain injury (TBI) involves both primary mechanical damage and refractory secondary injuries, resulting in high disability rate and poor prognosis. Current therapeutic strategies for TBI include surgical intervention, neuroprotective agents, moderate hypothermia therapy and spinal cord stimulation. However, most of these therapeutic approaches primarily address wound surface management rather than targeting specific pathogenic mechanisms underlying post-injury inflammation and neurodegenerative diseases, resulting in suboptimal efficacy. Consequently, novel therapeutic strategies targeting TBI pathological mechanisms are urgently needed. The endogenous cannabinoid system (ECS) exerts multifaceted neuroprotective effects in TBI by modulating neuroinflammation, inhibiting glutamate excitotoxicity and activating pathways such as phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt). Investigating the characteristics of ECS components and their related signaling pathways may yield new approaches in the development of neuroprotective drugs for TBI. Nevertheless, few ESC-targeting drugs for TBI treatment have advanced beyond preclinical or clinical trial phases. Breakthroughs in this field depend on a deeper understanding of ECS and its mechanisms in TBI. To this end, the authors reviewed researches on the composition and functions of ECS, as well as the mechanisms underlying its neuroprotective effects following TBI, aiming to provide references for the development of ECS-targeting therapies.

Objective To explore the value of inflammatory markers in predicting paroxysmal sympathetic hyperactivity(PSH)after traumatic brain injury(TBI).Methods A total of 84 TBI patients who were admitted to The Second Affiliated Hospital of Naval Medical University(Second Military Medical University)from Dec.2016 to Nov.2020 were retrospectively analyzed.They were classified into PSH group(n=41)and non-PSH group(n=43)according to whether PSH occurred during hospitalization.The baseline data and laboratory results of the 2 groups were collected and compared.Kendall correlation analysis was used to analyze the correlation between inflammatory markers and the occurrence of PSH after TBI,and receiver operating characteristic(ROC)curve was used to analyze the predictive value of inflammatory markers to PSH.Results There were no significant differences in baseline data,including age,gender,or Glasgow coma scale score,between the 2 groups(all P＞0.05).Compared with patients in the non-PSH group,the neutrophil to lymphocyte ratio(NLR),platelet to lymphocyte ratio(PLR),systemic immune-inflammation index(SII),neutrophils and leukocytes in the PSH group were significantly increased(all P＜0.05).NLR,SII and neutrophil were positively correlated with PSH(r=0.360,0.308,0.289;all P＜0.01),with the corresponding ROC area under curve values being 0.752,0.716 and 0.702,respectively.Conclusion NLR,SII and neutrophils have a value in predicting the occurrence of PSH after TBI.

Traumatic brain injury (TBI) involves both primary mechanical damage and refractory secondary injuries, resulting in high disability rate and poor prognosis. Current therapeutic strategies for TBI include surgical intervention, neuroprotective agents, moderate hypothermia therapy and spinal cord stimulation. However, most of these therapeutic approaches primarily address wound surface management rather than targeting specific pathogenic mechanisms underlying post-injury inflammation and neurodegenerative diseases, resulting in suboptimal efficacy. Consequently, novel therapeutic strategies targeting TBI pathological mechanisms are urgently needed. The endogenous cannabinoid system (ECS) exerts multifaceted neuroprotective effects in TBI by modulating neuroinflammation, inhibiting glutamate excitotoxicity and activating pathways such as phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt). Investigating the characteristics of ECS components and their related signaling pathways may yield new approaches in the development of neuroprotective drugs for TBI. Nevertheless, few ESC-targeting drugs for TBI treatment have advanced beyond preclinical or clinical trial phases. Breakthroughs in this field depend on a deeper understanding of ECS and its mechanisms in TBI. To this end, the authors reviewed researches on the composition and functions of ECS, as well as the mechanisms underlying its neuroprotective effects following TBI, aiming to provide references for the development of ECS-targeting therapies.

Traumatic brain injury (TBI) has been recognized as a risk factor for developing dementia. Currently, around 69 million people worldwide suffer from TBI each year, while the overall incidence of TBI among Chinese residents is on a rapid rise. Such a large population of TBI patients may lead to a future surge in the number of dementia patients, bringing heavy burdens on families and societies. However, it seems to be suggested by numerous studies that not all TBI patients are associated with an increased risk of dementia. Dementia can result in disability as well as interfere with caregivers ′ normal lives. Therefore, it will be significant to clarify the relationship between TBI and dementia as well as explain the process of onset and development of post-TBI dementia. In this study, the authors summarize post-TBI dementia from aspects of influencing factors and pathogenic mechanisms, so as to provide relevant references for related studies, therapy, and prophylaxis of post-TBI dementia.