Objective To evaluate the usefulness of quantitative electroencephalogram （QEEG）, flash visual evoked potential （F-VEP） and auditory brainstem responses （ABR） as indicators of general neurological status. Methods Comparison was conducted on healthy controls （N=30） and patients with brain concussion （N=60） within 24 h after traumatic brain injury. Follow-up study of patient group was completed with the same standard paradigm 3 months later. All participants were recorded in multi-modality related potential testing in both early and late concussion at the same clinical setting. Glasgow coma scale, CT scanning, and physical examinations of neuro-psychological function, optic and auditory nervous system were performed before electroencephalogram （EEG） and evoked potential （EEG-EP） testing. Any participants showed abnormal changes of clinical examinations were excluded from the study. Average power of frequency spectrum and power ratios were selected for QEEG testing, and latency and amplitude of F-VEP and ABR were recorded. Results Between patients and normal controls, the results indicated： （1） Highly significance （P 〈 0.01） in average power of α1 and power ratios of θ/α1, 0/α2, α1/α2 of EEG recording; （2） N70-P 100 amplitude of F-VEP in significant difference at early brain concussion; and （3） apparent prolongation of Ⅰ～Ⅲ inter-peak latency of ABR appeared in some individuals at early stage after concussion. The follow-up study showed that some patients with concussion were also afflicted with characteristic changes of EEG components for both increments of α1 average power and θ/α2 power ratio after 3 months recording. Conclusion EEG testing has been shown to be more effective and sensitive than evoked potential tests alone on detecting functional state of patients with mild traumatic brain injury （MTBI）. Increments of α1 average power and θ/α2 power ratio are the sensitive EEG parameters to determining early concussion and evaluating outcome of
It has been well established that the recovery ability of central nervous system （CNS） is very poor in adult mammals. As a result, CNS trauma generally leads to severe and persistent functional deficits. Thus, the investigation in this field becomes a ＂hot spot＂. Up to date, accumulating evidence supports the hypothesis that the failure of CNS neurons to regenerate is not due to their intrinsic inability to grow new axons, but due to their growth state and due to lack of a permissive growth environment. Therefore, any successful approaches to facilitate the regeneration of injured CNS axons will likely include multiple steps： keeping neurons alive in a certain growth-state, preventing the formation of a glial scar, overcoming inhibitory molecules present in the myelin debris, and giving direction to the growing axons. This brief review focused on the recent progress in the neuron regeneration of CNS in adult mammals.
NF-κB family is a kind of nuclear factors in B lymphocyte that can bind to the immunoglobulin κ-chain enhancer and enhance transcriptional activity. NF-κB/Rel proteins, as a dimeric transcription factor, control the expression of genes that regulate a broad range of biological processes through canonical and non-canonical pathways. In the central nervous system, NF-κB controls inflammatory reactions and the apoptotic cell death following nerve injury. It also contributes to the infarction and cell death in stroke models and patients. However, NF-κB is essential for neurosurvival as well. NF-κB activation is a part of recovery process that may protect neurons against oxidative-stresses or brain ischemia-induced apoptosis and neurodegeneration. Inhibition of NF-κB may reduce its neuroprotection activity. Hence the dual opposite effects of NF-κB on cells. The ultimate survival or death of neurons depends on which, where and when the NF-κB factors are activated.
Objective To investigate changes of autophagy after traumatic brain injury （TBI） and its possible role. Methods Rat TBI model was established by controlled cortical injury system. Autophagic double membrane structure was detected by transmission electronic microscope. Microtubule-associated protein 1 light chain 3 （LC3） and Beclin 1 were also used to investigate the activation of autophagy post-TBI. Double labeling with LC3 and caspase-3, or Beclin 1 and Fluoro-Jade, to show the relationship between autophagy and apoptosis or neuron degeneration after TBI. Results An increase of autophagic double membrane structure was observed in early stage （1 h）, and the increase lasted for at least 32 d post-TBI. LC3 and Beclin 1 proteins also began to elevate at 1 h time point post-TBI in neurons, 3 d later in astrocytes, and peaked at about 8 d post-TBI. In both cell types, LC3 and Beclin l maintained at a high level until 32 d post-TBI. Most LC3 and Beclin 1 positive cells were near the side （including hippocampus）, but not in the core of the injury. In addition, in the periphery of the injury site, not all caspase-3 positive （＋） cells merged with LC3 （＋） cells post-TBI; In hippocampal area, almost all Beclin 1 （＋） neurons did not merge with Fluoro-Jade （＋） neurons from 1 h to 48 h post-TBI. Conclusion Autophagy is activated and might protect neurons from degeneration at early stage post-TBI and play a continuous role afterwards in eliminating aberrant cell components.
