OBJECTIVES: To investigate the characteristics and objective assessment method of visual field defects caused by optic chiasm and its posterior visual pathway injury. METHODS: Typical cases of visual field defects caused by injuries to the optic chiasm, optic tracts, optic radiations, and visual cortex were selected. Visual field examinations, visual evoked potential (VEP) and multifocal visual evolved potential (mfVEP) measurements, craniocerebral CT/MRI, and retinal optical coherence tomography (OCT) were performed, respectively, and the aforementioned visual electrophysiological and neuroimaging indicators were analyzed comprehensively. RESULTS: The electrophysiological manifestations of visual field defects caused by optic chiasm injuries were bitemporal hemianopsia mfVEP abnormalities. The visual field defects caused by optic tract, optic radiation, and visual cortex injuries were all manifested homonymous hemianopsia mfVEP abnormalities contralateral to the lesion. Mild relative afferent pupil disorder (RAPD) and characteristic optic nerve atrophy were observed in hemianopsia patients with optic tract injuries, but not in patients with optic radiation or visual cortex injuries. Neuroimaging could provide morphological evidence of damages to the optic chiasm and its posterior visual pathway. CONCLUSIONS Visual field defects caused by optic chiasm, optic tract, optic radiation, and visual cortex injuries have their respective characteristics. The combined application of mfVEP and static visual field measurements, in combination with neuroimaging, can maximize the assessment of the location and degree of visual pathway damage, providing an effective scheme for the identification of such injuries.
Humans ; Optic Chiasm/pathology* ; Visual Pathways/pathology* ; Visual Fields ; Evoked Potentials, Visual ; Random Amplified Polymorphic DNA Technique ; Hemianopsia/complications* ; Vision Disorders/pathology* ; Optic Nerve Injuries/diagnostic imaging* ; Brain Injuries, Traumatic/diagnostic imaging*

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

OBJECTIVETo investigate the protective effect of prostaglandin E1 (PGE-1) against brain injury induced by hyperoxia in neonatal rats and observe the changes in the expression of glucose-regulated protein 78 (GRP78) and cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), and to provide a theoretical basis for the clinical application of PGE-1 in the treatment of neonatal brain injury induced by hyperoxia.

METHODSSixty neonatal Wistar rats were randomly divided into air control group, hyperoxic brain injury model group, and hyperoxic brain injury+PGE-1 group. All rats except those in the air control group were treated to establish a hyperoxic brain injury model. From the first day of modeling, the rats in the hyperoxia brain injury+PGE-1 group were intraperitoneally injected with PGE-1 2 μg/kg daily for 7 consecutive days, while the other two groups were treated with normal saline instead. The water content of brain tissue was measured; the pathological changes of brain tissue were evaluated by hematoxylin-eosin staining; the apoptosis of brain cells was assessed by nuclear staining combined with TUNEL staining; the protein expression of GRP78 and CHOP in brain tissue was measured by Western blot.

RESULTSThe water content of brain tissue in the hyperoxic brain injury model group was significantly higher than that in the hyperoxic brain injury+PGE-1 group and air control group (P<0.05); the water content of brain tissue in the hyperoxic brain injury+PGE-1 group was significantly higher than that in the air control group (P<0.05). The pathological section of brain tissue showed inflammatory cell infiltration and mild cerebrovascular edema in the brain parenchyma in the hyperoxic brain injury model group; the periparenchymal inflammation and edema in the hyperoxic brain injury+PGE-1 group were milder than those in the hyperoxic brain injury model group. The apoptosis index of brain tissue in the hyperoxic brain injury model group was significantly higher than that in the hyperoxic brain injury+PGE-1 group and air control group (P<0.05); the apoptosis index of brain tissue in the hyperoxic brain injury+PGE-1 group was significantly higher than that in the air control group (P<0.05). The protein expression of GRP78 and CHOP in brain tissue was significantly higher in the hyperoxic brain injury model group than in the hyperoxic brain injury+PGE-1 group and air control group (P<0.05); the protein expression of GRP78 and CHOP was significantly higher in the hyperoxic brain injury+PGE-1 group than in the air control group (P<0.05).

CONCLUSIONSPGE-1 has a protective effect against hyperoxia-induced brain injury in neonatal rats, which may be related to the inhibition of cell apoptosis by down-regulating the expression of GRP78 and CHOP.

Alprostadil ; therapeutic use ; Animals ; Animals, Newborn ; Apoptosis ; drug effects ; Brain ; pathology ; Brain Injuries ; metabolism ; pathology ; prevention & control ; Heat-Shock Proteins ; analysis ; Hyperoxia ; complications ; Neuroprotective Agents ; therapeutic use ; Rats ; Rats, Wistar ; Transcription Factor CHOP ; analysis

OBJECTIVETo examine the effect of icariin (ICA) on the cognitive impairment induced by traumatic brain injury (TBI) in mice and the underlying mechanisms related to changes in hippocampal acetylation level.

METHODSThe modifified free-fall method was used to establish the TBI mouse model. Mice with post-TBI cognitive impairment were randomly divided into 3 groups using the randomised block method (n=7): TBI (vehicle-treated), low-dose (75 mg/kg) and high-dose (150 mg/kg) of ICA groups. An additional sham-operated group (vehicle-treated) was employed. The vehicle or ICA was administrated by gavage for 28 consecutive days. The Morris water maze (MWM) test was conducted. Acetylcholine (ACh) content, mRNA and protein levels of choline acetyltransferase (ChAT), and protein levels of acetylated H3 (Ac-H3) and Ac-H4 were detected in the hippocampus.

RESULTSCompared with the sham-operated group, the MWM performance, hippocampal ACh content, mRNA and protein levels of ChAT, and protein levels of Ac-H3 and Ac-H4 were signifificantly decreased in the TBI group (P<0.05). High-dose of ICA signifificantly ameliorated the TBI-induced weak MWM performance, increased hippocampal ACh content, and mRNA and protein levels of ChAT, as well as Ac-H3 protein level compared with the TBI group (P<0.05).

CONCLUSIONICA improved post-TBI cognitive impairment in mice by enhancing hippocampal acetylation, which improved hippocampal cholinergic function and ultimately improved cognition.

Acetylation ; Acetylcholine ; metabolism ; Animals ; Brain Injuries, Traumatic ; complications ; Choline O-Acetyltransferase ; genetics ; metabolism ; Cognitive Dysfunction ; drug therapy ; etiology ; Flavonoids ; chemistry ; pharmacology ; therapeutic use ; Hippocampus ; pathology ; Histones ; metabolism ; Homeostasis ; drug effects ; Male ; Maze Learning ; drug effects ; Mice ; RNA, Messenger ; genetics ; metabolism

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 explore the relationship between histological chorioamnionitis (HCA) and fetal inflammatory response syndrome (FIRS) and brain injury in preterm infants.

METHODSOne hundred and three singleton infants with premature rupture of membranes (PROM) (gestation ages of less than 34 weeks) were enrolled. All the placentas were submitted for pathological evaluation. Umbilical cord blood interleukin 6 (IL-6), interleukin 8 (IL-8), tumor necrosis factor alpha (TNF-α) and granulocyte-colony stimulating factor (G-CSF) levels were measured with liquid chip. All preterm infants accepted brain imaging examinations. Based on the placental pathological examination and umbilical cord blood level of IL-6, the 103 infants were classified into HCA⁻ FIRS⁻, HCA⁺ FIRS⁻, and HCA⁺ FIRS⁺ groups.

RESULTSThe incidences of HCA, FIRS, and brain injury were 53.4%, 20.4% and 38.8% respectively. The prevalence of brain injury in HCA⁻ FIRS⁻, HCA⁺ FIRS⁻, and HCA⁺ FIRS⁺ cases was 21%, 41%, and 76% respectively (P<0.01). The grade 2 and grade 3 of placental inflammation and the inflammation at stage 2 and stage 3 increased the risk of brain injury. The cord blood levels of IL-8, TNF-α, and G-CSF in the HCA⁺ FIRS⁺ group were significantly higher than in the other two groups, and the levels of the above parameters in the HCA⁺ FIRS⁻ were higher than in the HCA⁻ FIRS⁻ group (P<0.05).

CONCLUSIONSPlacental inflammation and FIRS are associated with brain injury in preterm infants. Preterm infants exposed to severe placental inflammation have an increased risk of brain injury. Cord blood IL-8, TNF-α and G-CSF may be involved in the process of brain injury in preterm infants with placental inflammation and FIRS.

Brain Injuries ; etiology ; Chorioamnionitis ; pathology ; Female ; Granulocyte Colony-Stimulating Factor ; blood ; Humans ; Infant, Newborn ; Infant, Premature ; Inflammation ; complications ; Interleukin-8 ; blood ; Male ; Placenta ; pathology ; Pregnancy ; Tumor Necrosis Factor-alpha ; blood

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 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

OBJECTIVETo investigate the risk factors of progressive brain contusion and to evaluate their impact on patients' outcome.

METHODSOne hundred and thirty two patients with traumatic brain contusion were enrolled in the study, including 70 cases with progressive contusion and 62 cases with non-progressive contusion. The risk factors were investigated with univariate and multivariate Logistic regression analysis.

RESULTSThe univariate analysis showed that Glasgow Coma Score (GCS) at admission, contusion volume at the first brain CT scans, midline shift, combined with skull fracture, subarachnoid hemorrhage, epidural hematoma, subdural hematoma, location of brain contusion, D-dimer levels, combined with type 2 diabetes were associated with progressive brain contusion. Multivariate Logistic regression analysis showed that GCS at admission, contusion volume at the first CT scans, combined with subarachnoid hemorrhage, combined with type 2 diabetes were the independent risk factors for disease progression. The outcome in the progressive group was more aggravated than that in non-progressive group (P = 0.001).

CONCLUSIONPatients with disturbance of consciousness, the larger contusion volume, combined with subarachnoid hemorrhage and diabetes are at risk for progressive brain contusion and unfavorable outcome.

Brain Injuries ; complications ; pathology ; Diabetes Mellitus, Type 2 ; complications ; Disease Progression ; Fibrin Fibrinogen Degradation Products ; metabolism ; Glasgow Coma Scale ; Hematoma, Epidural, Cranial ; complications ; Hematoma, Subdural ; complications ; Humans ; Risk Factors ; Subarachnoid Hemorrhage ; complications ; Tomography, X-Ray Computed

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