Visual event-related potential (ERP) is an electrophysiological technique that objectively reflects the cognitive processing of stimulus from the perspective of detecting and recording neural electrophysiology responses using different paradigms of visual stimuli. Its endogenous components are closely related to advanced psychological activities. This article introduces the characteristics of main endogenous components including visual mismatch negativity (vMMN), N200 and P300, reviews the research progress of visual ERP in the sequelae of brain injury and objective evaluation of visual function, and prospects the application prospect of visual ERP in the field of forensic medicine.
Humans ; Brain Injuries, Traumatic/complications* ; Evoked Potentials ; Brain Injuries ; Forensic Medicine

Brain Injuries ; etiology ; Child ; Heart Defects, Congenital ; complications ; Humans

Brain Injuries ; etiology ; prevention & control ; Humans ; Hyperbilirubinemia ; complications ; prevention & control

Brain Injuries ; etiology ; Humans ; Hypoglycemia ; complications ; Infant, Newborn

Neurosurgical emergencies including intracranial hemorrhage and head trauma have high mortality and morbidity rates and meanwhile are often accompanied with coagulation disorders. On one hand, coagulation disorder follows traumatic brain injury;on the other hand, the increasing use of anticoagulant and antiplatelet treatment for cardiovascular diseases increases the risk of death among patients with brain trauma or bleeding. Once the intracranial pressure increases, such patients need emergency surgical intervention, but coagulation disorder is a relative contraindication. This article reviews the pathogenesis and treatment of coagulation disorders in patients with neurosurgical emergency. It also analyzes clinical monitoring indices for such patients and their variations and summarizes the strategies and measures of perioperative management.
Blood Coagulation Disorders ; complications ; physiopathology ; surgery ; Brain Injuries ; complications ; surgery ; Emergencies ; Humans ; Intracranial Hemorrhages ; complications ; surgery

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

Mild traumatic brain injury (MTBI) is defined as a mild brain trauma resulting in a short loss of consciousness and alteration of mental status. It may also occasionally develop persistent and progressive symptoms. It has been confirmed that MTBI causes changes of anatomic structures in central nervous system and biomarkers in the body fluid. However, there is no sufficient research on relevance among threshold for the brain injury, individual vulnerability and duration of disturbance of consciousness. Furthermore, there are no reliable diagnostic methods to establish whether a blow to the head is sufficient to cause the brain injury. This review provides references for biomarkers in cerebrospinal fluid and blood associated with TBI. It also provides application status and potential prospects for further assessment and diagnosis of MTBI.
Biomarkers/cerebrospinal fluid* ; Brain Concussion/complications* ; Brain Injuries/etiology* ; Disease Progression ; Humans

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

Blast injury has become the major life- and function-threatening injuries in recent warfares. There is increased research interest in the mental disorders caused by blast-induced traumatic brain injury (bTBI), which has been proved as one of the "signature wounds" in modern battlefield. We reviewed the recent progresses in bTBI-related researches and concluded that the new era of blast injury research has shifted from the traditional physical impairments to cognitive dysfunctional/mental disorders that are proved to be more related to the outcome of combat casualty care.
Animals ; Blast Injuries ; complications ; etiology ; Brain Injuries, Traumatic ; complications ; etiology ; Cognition Disorders ; etiology ; Humans ; Mental Disorders ; etiology ; Research

Brain edema leading to an expansion of brain volume has a crucial impact on morbidity and mortality following traumatic brain injury as it increases intracranial pressure, impairs cerebral perfusion and oxygenation, and contributes to additional ischemic injuries. Classically, two major types of traumatic brain edema exist: "vasogenic" and "cytotoxic/cellular". However, the cellular and molecular mechanisms contributing to the development/resolution of traumatic brain edema are poorly understood and no effective drugs can be used now. Aquaporin-4 (AQP4) is a water-channel protein expressed strongly in the brain, predominantly in astrocyte foot processes at the borders between the brain parenchyma and major fluid compartments, including cerebrospinal fluid and blood. This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma. In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma. AQP4 has been proposed as a novel drug target in brain edema. These findings suggest that modulation of AQP4 expression or function may be beneficial in traumatic brain edema.
Animals ; Aquaporin 4 ; analysis ; antagonists & inhibitors ; chemistry ; physiology ; Brain ; metabolism ; Brain Edema ; drug therapy ; etiology ; Brain Injuries ; complications ; Humans ; Mice