Brainstem of rats were stabbed with a needle and pathological changes of neurons and axons in brainstem were observed at different time after injury with Nissl's body staining, silver staining and modified trichrome staining. It was found that, by silver staining, the axons showed irregular swelling and disconnection at 1-3 h, marked swelling of the severe end at 6 h, retraction ball at 15 h and remarkable retraction ball at 24 h. By modified trichrome staining, the space between myelin sheaths and axons was widened at 3-6 h, and tortuous myelin sheaths adhered incompletely on axons, or even peeled off at 15 h to 24 h. Perinuclear lysis of Nissl's bodies at 24 h after injury could be seen by Nissl body staining. The results indicated that, the pathological changes in injured brainstem could be observed with histochemical staining, which might be used for timing brainstem injuries.
Animals ; Axons/pathology* ; Brain Injuries/pathology* ; Brain Stem/injuries* ; Female ; Histocytochemistry ; Male ; Neurons/pathology* ; Rats ; Rats, Wistar ; Staining and Labeling

Brain Injuries ; blood ; Humans ; Hypoglycemia ; pathology ; Infant, Newborn ; Infant, Premature

TAR DNA-binding domain protein 43 （TDP-43） is a highly conserved and widely expressed nuclear protein. Nowadays, the expression of TDP-43 can be found in most neurodegenerative diseases such as Alzheimer's disease, which makes it become a neurodegenerative disease associated marker protein. From the current research status at homeland and abroad, and around the relationship between the expression of TDP-43 and brain injury, this article emphatically probes into the specific expression and function of TDP-43 in acute and chronic brain injury based on the knowledge of its biological characteristics, which aims to explore the feasibility for determining the cause of death and the injury and disability situations by TDP-43 in forensic pathology.
Brain Injuries/pathology* ; DNA ; DNA-Binding Proteins/metabolism* ; Humans

OBJECTIVEFollowing traumatic brain injury (TBI), brain tissue that surrounding the regional primary lesion is known as traumatic penumbra; this region may undergo secondary injury and is considered to have the potential to recover. This review aimed to reveal the existence and significance of traumatic penumbra by analyzing all relevant studies concerning basic pathologic changes and brain imaging after TBI.

DATA SOURCESWe collected all relevant studies about TBI and traumatic penumbra in Medline (1995 to June 2013) and ISI (1997 to March 2013), evaluated their quality and relevance, then extracted and synthesized the information.

STUDY SELECTIONWe included all relevant studies concerning TBI and traumatic penumbra (there was no limitation of research design and article language) and excluded the duplicated articles.

RESULTSThe crucial pathological changes after TBI include cerebral blood flow change, cerebral edema, blood-brain barrier damage, cell apoptosis and necrosis. Besides, traditional imaging method cannot characterize the consequences of CBF reduction at an early stage and provides limited insights into the underlying pathophysiology. While advanced imaging technique, such as diffusion tensor imaging (DTI) and positron emission tomography (PET), may provide better characterization of such pathophysiology.

CONCLUSIONSThe future of traumatic brain lesions depends to a large extent on the evolution of the penumbra. Therefore, understanding the formation and pathophysiologic process of the traumatic penumbra and its imaging research progress is of great significant for early clinical determination and timely brain rescue.

Animals ; Apoptosis ; physiology ; Brain ; pathology ; Brain Injuries ; complications ; pathology ; Cerebrovascular Circulation ; physiology ; Humans ; Necrosis ; physiopathology

The brain pericyte is a unique and indispensable part of the blood-brain barrier (BBB), and contributes to several pathological processes in traumatic brain injury (TBI). However, the cellular and molecular mechanisms by which pericytes are regulated in the damaged brain are largely unknown. Here, we show that the formation of neutrophil extracellular traps (NETs) induces the appearance of CD11b⁺ pericytes after TBI. These CD11b⁺ pericyte subsets are characterized by increased permeability and pro-inflammatory profiles compared to CD11b^- pericytes. Moreover, histones from NETs by Dectin-1 facilitate CD11b induction in brain pericytes in PKC-c-Jun dependent manner, resulting in neuroinflammation and BBB dysfunction after TBI. These data indicate that neutrophil-NET-pericyte and histone-Dectin-1-CD11b are possible mechanisms for the activation and dysfunction of pericytes. Targeting NETs formation and Dectin-1 are promising means of treating TBI.
Blood-Brain Barrier/metabolism* ; Brain/pathology* ; Brain Injuries, Traumatic/metabolism* ; Extracellular Traps/metabolism* ; Histones ; Humans ; Lectins, C-Type ; Pericytes/pathology*

OBJECTIVETo investigate the influence of therapeutic bloodletting at Jing-well points and hypothermia on acute cerebral edema after traumatic brain injury (TBI) in rats.

METHODSSeventy-five SD rats were randomly divided into sham-operation group (Sham), TBI group (TBI), bloodletting group (BL), mild-induced hypothermia group (MIH), and bloodletting plus MIH group (BL + MIH) (n = 15). The model of TBI was established by electric controlled cortical impactor (eCCI). The rats of BL group were bloodletting at Jing-well points immediately after injury, twice daily. While the MIH group was settled on a hypothermia blanket promptly after TBI for 6 hours, so that the temperature dropped to 32 degrees. Each of measurement was performed after 48 hours. Magnetic resonance imaging (MRI) was used to evaluate the dynamic impairment of cerebral edema after TBI (n = 3). In addition, mNSS score, measurements of wet and dry brain weight, and Evans Blue assay were performed to investigate the neurologic deficit, cerebral water content (n = 8), and blood-brain barrier permeability (BBB), (n = 4), respectively.

RESULTSMRI analysis showed that the cerebral edema, hematoma and midline shifting of rats in TBI group was more serious than other treatment group. Meanwhile compared with TBI group, the mNSS scores of every treatment group were meaningfully lower (all P < 0.05). Furthermore, treatment with BL+ MIH group was superior to the separated BL and MIH group (all P < 0.01). In addition, brain water content of each intervention group reduced to varying degrees (all P < 0.05), especially that of MIH group and BL + MIH group (P <0.01). BBB permeability of each treatment group was also significantly improved (all P < 0.01), and the improvement in MIH group and BL + MIH group was much better than the BL alone group (P < 0.05, P < 0.01).

CONCLUSIONOur major finding is that bloodletting at Jing-well points and MIH can reduce cerebral edema and BBB dysfunction and exert neuroprotective effects after TBI. The results suggest that the combination of BL and MIH is more effective than other treatment being used alone.

Animals ; Blood-Brain Barrier ; Bloodletting ; Brain ; pathology ; Brain Edema ; prevention & control ; Brain Injuries ; therapy ; Hypothermia, Induced ; Rats ; Rats, Sprague-Dawley

OBJECTIVES: To study the forensic features of diffuse brain atrophy after trauma, the relationship between age and interval time of post-traumatic brain atrophy, and the relationship between the degree of craniocerebral injury and that of brain atrophy. METHODS: The forensic features of 25 cases of diffuse brain atrophy after craniocerebral trauma were retrospectively analyzed from aspects of gender, age, craniocerebral injury characteristics, and imaging characteristics of brain atrophy. Pearson correlation analysis was used for statistical analysis. RESULTS: Diffuse brain atrophy after trauma could occur in any age group, dominated by severe brain injury. The Pearson correlation coefficients （r） between the time interval of brain atrophy and age were 0.442 （ P<0.05）, 0.341 （P>0.05）, and 0.904 （ P<0.05） for the overall cases, the group over age 50, and the group under age 50, respectively. The correlation coefficient between the degree of brain injury and that of brain atrophy was 0.579 （ P<0.05）, and that between severe brain injury and brain atrophy was 0.788 （ P<0.05）. CONCLUSIONS The more serious the brain injury, the more severe the brain atrophy. Various degrees of diffuse brain atrophy can occur in severe craniocerebral injury, and diffuse brain atrophy is usually mild and moderate after mild and moderate craniocerebral injury. In the practice of forensic clinical identification, a comprehensive analysis should be conducted with the combination of case materials when the identified person has high risk factors leading to brain atrophy （e.g., hypertension, diabetes, etc.）, plus injury and illness relationship analysis if necessary.
Atrophy ; Brain/pathology* ; Brain Injuries/complications* ; Craniocerebral Trauma ; Humans ; Retrospective Studies

It is the intent of this study to estimate the progression or regression of edema at the bedside continuously. Based on the theoretic model, the Adaptive Genetic Algorithm (AGA) has been applied in the calculation of conductivity reconstruction. Dynamic crossover and mutation operators which are based on Haiming Distance are brought forward in this paper to maintain generation's diversity. Then, both AGA and Standard GA (SGA) have been applied in the conductivity reconstruction of edema in human brain. It is shown that AGA not only has attained a higher degree of efficiency but also has enhanced the capability to converge to the best answer.
Algorithms ; Brain Injuries ; complications ; pathology ; Computer Simulation ; Edema ; pathology ; Electric Impedance ; Humans ; Models, Biological

Adult ; Brain ; pathology ; physiology ; Humans ; Magnetic Resonance Imaging ; Male ; Spinal Cord Injuries ; pathology ; physiopathology

The evidence and the feature of apoptosis following tyrauma brain injury(TBI) and the possible mechanisms underlying apoptosis were reviewed. Recently research showed that apoptosis play an important role in TBI, the occurring time and area of apoptosis were found significant differences compared with that of necrosis. The neural cell apoptosis can undergo following many pathways after TBI. In our review, the foreground of apoptosis after TBI research in forensic pathology were also discussed.
Animals ; Apoptosis/physiology* ; Brain Injuries/pathology* ; Forensic Medicine ; Gene Expression Regulation ; Humans ; Neurons/pathology*