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

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

PURPOSEWe once reported blast-induced traumatic brain injury (bTBI) in confined space. Here, bTBI was studied again on goats in the open air using 3.0 kg trinitrotoluene.

METHODSThe goats were placed at 2, 4, 6 and 8 m far from explosion center. Trinitrotoluene (TNT) was used as the source of the blast wave and the pressure at each distance was recorded. The systemic physiology, electroencephalogram, serum level of S-100 beta, and neuron specific enolase (NSE) were determined pre and post the exposure. Neuroanatomy and neuropathology were observed 4 h after the exposure.

RESULTSSimple blast waveforms were recorded with parameters of 702.8 kPa-0.442 ms, 148.4 kPa-2.503 ms, 73.9 kPa-3.233 ms, and 41.9 kPa-5.898 ms at 2, 4, 6 and 8 m respectively. Encephalic blast overpressure was on the first time recorded in the literature by us at 104.2 kPa-0.60 ms at 2 m, where mortality and burn rate were 44% and 44%. Gross examination showed that bTBI was mainly manifested as congestive expansion of blood vessels and subarachnoid hemorrhage, which had a total incidence of 25% and 19% in 36 goats. Microscopical observation found that the main pathohistological changes were enlarged perivascular space (21/36, 58%), small hemorrhages (9/36, 25%), vascular dilatation and congestion (8/36, 22%), and less subarachnoid hemorrhage (2/36, 6%). After explosion, serum levels of S-100b and NSE were elevated, and EEG changed into slow frequency with declined amplitude. The results indicated that severity and incidence of bTBI is related to the intensity of blast overpressure.

CONCLUSIONBlast wave can pass through the skull to directly injure brain tissue.

Animals ; Blast Injuries ; complications ; Brain ; pathology ; Brain Injuries, Traumatic ; etiology ; pathology ; Electroencephalography ; Goats ; Male ; Phosphopyruvate Hydratase ; blood ; S100 Calcium Binding Protein beta Subunit ; blood

OBJECTIVETo explore the features of rats organs functional changes after femur shaft fracture combined with brain injury through testing biochemical indicators in rats.

METHODSThirty 4-month-old male SD rats, weight (280 +/- 10) g, were divided into 5 groups according to random number table involving normal control group, at the 1st day of injured group, the 2nd day injured group, the 3rd day injured group, the 5th day injured group, the 7th day injured group, 5 rats in each group. The animal injury model of right femur shaft fracture combined with brain injury were made by instruments in 5 injured groups. At the 1st, 2nd, 3rd, 5th, 7th day after made model, the biochemical indicators of blood serum from abdominal aorta including AST, ALT ,Cr, BUN, LDH and CK were detected and compared.

RESULTSThe biochemical indicator of blood serum (AST, ALT, Cr, BUN, LDH, CK) changed significantly among different groups. AST, ALT, BUN and CK reached peaks at the 1st day after injured (P<0.05). Cr reached peaks at the 3rd day after injured (P<0.05). LDH reached peak at the 2nd day after injured (P<0.05).

CONCLUSIONAfter brain injury combined with right femoral fractures in rats, a variety of serum biochemical indicators increase significantly, especially in early 3 days after injured. These indicators shows indirectly heart, liver and kidney organ dysfunction by trauma.

Animals ; Brain Injuries ; complications ; Femoral Fractures ; complications ; Male ; Multiple Organ Failure ; etiology ; metabolism ; pathology ; physiopathology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the value of susceptibility weighted imaging(SWI)in the diagnosis of hemorrhagic foci early after blast injury and its role in the outcome prediction.

METHODSTotally 30 rabbits with blast-induced cerebral blast injury were used in this study. After routine CT/MRI and SWI scanning,quantified analysis was performed in regions of interest using post-processing technology. After dissecting the brains of the experimental rabbits,the cerebral histopathological changes were observed,and the results were compared with SWI findings.

RESULTSIn these 30 rabbits,22,102,221,and 738 hemorrhagic foci were detected by CT,T1WI,T2WI,and SWI,respectively. The number of cerebral microbleeds detected by SWI was significantly larger than those revealed by conventional T1WI and T2WI(Χ(2)=10.00,P<0.01). Furthermore,the SWI imaging displayed the punctiform(n=315,42.7%),lamellar(n=218,29.5%),slinar(n=205,27.8%)hypointense foci,with clear margin. The number of hemorrhagic foci detected by SWI was positively correlated with survival(r=-0.667,P<0.05).

CONCLUSIONSSWI remarkably increases the detection rate of hemorrhagic foci(particularly microbleeds)in rabbits with cerebral blast injury. The number of cerebral microbleeds and location of foci are closely related with the outcomes and therefore may facilitate clinical managment.

Animals ; Blast Injuries ; complications ; diagnosis ; Brain ; pathology ; Brain Injuries ; diagnosis ; etiology ; Cerebral Hemorrhage ; diagnosis ; etiology ; Female ; Image Enhancement ; Magnetic Resonance Imaging ; methods ; Male ; Prognosis ; Rabbits

OBJECTIVETo characterize the expression of aquaporin-4 (AQP4), one of the aquaporins (AQPs), in human brain specimens from patients with traumatic brain injury or brain tumors.

METHODSNineteen human brain specimens were obtained from the patients with traumatic brain injury, brain tumors, benign meningioma or early stage hemorrhagic stroke. MRI or CT imaging was used to assess brain edema. Hematoxylin and eosin staining were used to evaluate cell damage. Immunohistochemistry was used to detect the AQP4 expression.

RESULTSAQP4 expression was increased from 15 h to at least 8 d after injury. AQP4 immunoreactivity was strong around astrocytomas, ganglioglioma and metastatic adenocarcinoma. However, AQP4 immunoreactivity was only found in the centers of astrocytomas and ganglioglioma, but not in metastatic adenocarcinoma derived from lung.

CONCLUSIONAQP4 expression increases in human brains after traumatic brain injury, within brain-derived tumors, and around brain tumors.

Adult ; Aged ; Aged, 80 and over ; Aquaporin 4 ; Aquaporins ; metabolism ; Biomarkers ; metabolism ; Brain Edema ; etiology ; metabolism ; pathology ; Brain Injuries ; complications ; metabolism ; pathology ; Brain Neoplasms ; complications ; metabolism ; pathology ; Female ; Humans ; Male ; Middle Aged ; Tissue Distribution

OBJECTIVETo explore the correlation between cognition disorder and morphologic change of hippocampal neurons after traumatic brain injury (TBI).

METHODSWistar rat models with severe TBI were made by Marmarou's method. The histopathological change of the neurons in the hippocampus area were studied with hematoxylin-eosin (HE) staining and terminal deoxynucleotidyl transferase-mediated X-dUPT nick end labeling (TUNEL), respectively. The cognitive function was evaluated with the Morris water maze test.

RESULTSThe comprehensive neuronal degeneration and necrosis could be observed in CA2-3 regions of hippocampus at 3 days after injury. Apoptotic positive neurons in CA2-4 regions of hippocampus and dentate gyrus increased in the injured group at 24 hours following TBI. They peaked at 7 days and then declined. Significant impairment of spatial learning and memory was observed after injury in the rats.

CONCLUSIONSThe rats have obvious disorders in spatial learning and memory after severe TBI. Meanwhile, delayed neuronal necrosis and apoptosis can be observed in the neurons in the hippocampus area. It suggests that delay ed hippocampal cell death may contribute to the functional deficit.

Animals ; Apoptosis ; Brain Injuries ; complications ; pathology ; Cognition Disorders ; etiology ; pathology ; Hippocampus ; pathology ; In Situ Nick-End Labeling ; Male ; Memory Disorders ; etiology ; pathology ; Necrosis ; Rats ; Rats, Wistar

Early brain injury (EBI) plays a key role in the pathogenesis of subarachnoid hemorrhage (SAH). This study investigated the role of glucose-regulated protein 78 (GRP78) in EBI after SAH. Male Sprague-Dawley rats (n=108) weighing 260±40 g were divided into control, sham-operated, and operated groups. Blood was injected into the prechiasmatic cistern of rats in the operated group. Neurological scores, ultrastructures of neurons, apoptosis, and GRP78 expression in the hippocampus were examined using Garcia scoring system, transmission electron microscopy, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling, and Western blotting at 1, 6, 12, 24, 48, and 72 h after SAH, respectively. The results showed that neurological scores were significantly decreased in the operated group as compared with those in control and sham-operated groups at 12, 24, 48, and 72 h. Metachromatin, chromatin pyknosis at the edge, endoplasmic reticulum swelling, and invagination of nuclear membrane were observed at 24 h in the operated group, indicating the early morphological changes of apoptosis. The number of apoptotic cells was significantly increased in the operated group as compared with that in control and sham-operated groups at 6, 12, 24, 48, and 72 h. The GRP78 protein expression levels in the operated group were significantly elevated at all time points and reached the peak at 12 h. GRP78 expression was positively associated with apoptosis cells and negatively with neurological scores. In conclusion, EBI was demonstrated to occur after SAH and GRP78 was involved in the development of EBI after SAH.
Animals ; Apoptosis ; Brain Injuries ; complications ; metabolism ; pathology ; Chromatin ; pathology ; Endoplasmic Reticulum Stress ; Heat-Shock Proteins ; genetics ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Subarachnoid Hemorrhage ; etiology ; metabolism ; pathology

OBJECTIVETo investigate the effects of three different ways of chronic caffeine administration on blast- induced memory dysfunction and to explore the underlying mechanisms.

METHODSAdult male C57BL/6 mice were used and randomly divided into five groups: control: without blast exposure, con-water: administrated with water continuously before and after blast-induced traumatic brain injury (bTBI), con-caffeine: administrated with caffeine continuously for 1 month before and after bTBI, pre-caffeine: chronically administrated with caffeine for 1 month before bTBI and withdrawal after bTBI, post-caffeine: chronically administrated with caffeine after bTBI. After being subjected to moderate intensity of blast injury, mice were recorded for learning and memory performance using Morris water maze (MWM) paradigms at 1, 4, and 8 weeks post-blast injury. Neurological deficit scoring, glutamate concentration, proinflammatory cytokines production, and neuropathological changes at 24 h, 1, 4, and 8 weeks post-bTBI were examined to evaluate the brain injury in early and prolonged stages. Adenosine A1 receptor expression was detected using qPCR.

RESULTSAll of the three ways of chronic caffeine exposure ameliorated blast-induced memory deficit, which is correlated with the neuroprotective effects against excitotoxicity, inflammation, astrogliosis and neuronal loss at different stages of injury. Continuous caffeine treatment played positive roles in both early and prolonged stages of bTBI; pre-bTBI and post-bTBI treatment of caffeine tended to exert neuroprotective effects at early and prolonged stages of bTBI respectively. Up-regulation of adenosine A1 receptor expression might contribute to the favorable effects of chronic caffeine consumption.

CONCLUSIONSince caffeinated beverages are widely consumed in both civilian and military personnel and are convenient to get, the results may provide a promising prophylactic strategy for blast-induced neurotrauma and the consequent cognitive impairment.

Animals ; Blast Injuries ; complications ; Brain Injuries, Traumatic ; complications ; Caffeine ; pharmacology ; Cerebral Cortex ; pathology ; Hippocampus ; pathology ; Male ; Memory Disorders ; etiology ; prevention & control ; Mice ; Mice, Inbred C57BL ; RNA, Messenger ; analysis ; Receptor, Adenosine A1 ; genetics