Purpose This study aimed to evaluate the impact of several factors, including patients' intraoperative position, intraoperative visualization technique, fixation method, and type of screws and their parameters, on the frequency of intraoperative screw-associated complications in posterior transarticular C1-C2 fixation. Methods A systematic review of the PubMed database between January 1986 and March 2018 was performed. The key inclusion criteria comprised detailed descriptions of the surgical technique and post-operative screw-associated complications. Results The initial search resulted in 1041 abstracts, and a total of 54 abstracts were included in the present study. The overall number of operated patients was 2306. In this group, 4439 screws were inserted. The rate of screw-associated complications during the different time periods was estimated upon meta-analysis. Statistical analysis of the screw malposition rate, vertebral artery injury rate, screw breakage rate based on patients' intraoperative position, intraoperative visualization technique, fixation method, and type of implants and their parameters was also performed. Conclusions The factors that help reduce the rate of screw-associated complications include the intraoperative application of biplanar fluoroscopy or neuronavigation system, the use of 4 mm or thicker lag screws, and screw insertion through contraincisions using cannulated ported instruments. On the other hand, the potential risk factors of screw-associated complications include inadequate intraoperative head fixation using skeletal traction, uniplanar fluoroscopy-guided screw insertion, screw insertion using the posterior midline approach, and the use of 3.5 mm or thinner full-threaded screws.Graphical abstract These slides can be retrieved under Electronic Supplementary Material.

Traumatic brain injury (TBI) is one of the major causes of death and disability in young and middle-aged people. The most problematic group is comprised of patients with severe TBI who are in a coma. The adequate diagnosis of primary brain injuries and timely prevention and treatment of the secondary injury mechanisms largely define the possibility of reducing mortality and severe disabling consequences. When developing these guidelines, we used our experience in the development of international and national recommendations for the diagnosis and treatment of mild traumatic brain injury, penetrating gunshot wounds to the skull and brain, severe traumatic brain injury, and severe consequences of brain injuries, including a vegetative state. In addition, we used international and national guidelines for the diagnosis, intensive care, and surgical treatment of severe traumatic brain injury, which had been published in recent years. The proposed guidelines concern intensive care of severe TBI in adults and are particularly intended for neurosurgeons, neurologists, neuroradiologists, anesthesiologists, and intensivists who are routinely involved in the treatment of these patients.

No abstract

Traumatic brain injury (TBI) is one of the main causes of mortality and severe disability in young and middle age patients. Patients with severe TBI, who are in coma, are of particular concern. Adequate diagnosis of primary brain injuries and timely prevention and treatment of secondary injury mechanisms markedly affect the possibility of reducing mortality and severe disability. The present guidelines are based on the authors' experience in developing international and national recommendations for the diagnosis and treatment of mild TBI, penetrating gunshot wounds of the skull and brain, severe TBI, and severe consequences of brain injury, including a vegetative state. In addition, we used the materials of international and national guidelines for the diagnosis, intensive care, and surgical treatment of severe TBI, which were published in recent years. The proposed recommendations for surgical treatment of severe TBI in adults are addressed primarily to neurosurgeons, neurologists, neuroradiologists, anesthesiologists, and intensivists who are routinely involved in treating these patients.

Background: In humans, early pathological activity on invasive electrocorticograms (ECoGs) and its putative association with pathomorphology in the early period of traumatic brain injury (TBI) remains obscure. Methods: We assessed pathological activity on scalp electroencephalograms (EEGs) and ECoGs in patients with acute TBI, early electrophysiological changes after lateral fluid percussion brain injury (FPI), and electrophysiological correlates of hippocampal damage (microgliosis and neuronal loss), a week after TBI in rats. Results: Epileptiform activity on ECoGs was evident in 86% of patients during the acute period of TBI, ECoGs being more sensitive to epileptiform and periodic discharges. A “brush-like” ECoG pattern superimposed over rhythmic delta activity and periodic discharge was described for the first time in acute TBI. In rats, FPI increased high-amplitude spike incidence in the neocortex and, most expressed, in the ipsilateral hippocampus, induced hippocampal microgliosis and neuronal loss, ipsilateral dentate gyrus being most vulnerable, a week after TBI. Epileptiform spike incidence correlated with microglial cell density and neuronal loss in the ipsilateral hippocampus. Conclusion: Epileptiform activity is frequent in the acute period of TBI period and is associated with distant hippocampal damage on a microscopic level. This damage is probably involved in late consequences of TBI. The FPI model is suitable for exploring pathogenetic mechanisms of post-traumatic disorders.