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*

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

OBJECTIVE: To investigate the effects of blocking the activation of ERK pathway on the expression of matrix metalloproteinase-9 (MMP-9) and the formation of cerebral edema in SD rats after brain injury. METHODS: Ninety SD rats were randomly divided into 3 equal groups, including a sham-operated group, modified Feeney's traumatic brain injury model group, and ERK inhibition group where the ERK inhibitor SCH772984 (500 μg/kg) was injected via the femoral vein 15 min before brain trauma. At 2 h and 2 days after brain trauma, the permeability of blood-brain barrier was assessed by Evans blue method, the water content of the brain tissue was determined, and the phosphorylation level of ERK and the expression level of MMP-9 mRNA and protein were measured by RT-PCR and Western blotting. RESULTS: Compared with the sham-operated group, the rats with brain trauma exhibited significantly increased level of ERK phosphorylation at 2 h and significantly increased expression of MMP-9 mRNA and protein 2 days after the injury ( < 0.01). Treatment with the ERK inhibitor significantly decreased the phosphorylation level of ERK after the injury ( < 0.01), suppressed over-expression of MMP-9 mRNA and protein 2 days after the injury ( < 0.01). The permeability of blood-brain barrier increased significantly 2 h after brain trauma ( < 0.05) and increased further at 2 days ( < 0.01); the water content of the brain did not change significantly at 2 h ( > 0.05) but increased significantly 2 d after the injury ( < 0.01). Treatment with the ERK inhibitor significantly lowered the permeability of blood-brain barrier and brain water content after brain trauma ( < 0.01). CONCLUSIONS Blocking the activation of ERK pathway significantly reduced the over-expression of MMP-9 and alleviates the damage of blood-brain barrier and traumatic brain edema, suggesting that ERK signaling pathway plays an important role in traumatic brain edema by regulating the expression of MMP-9.
Animals ; Brain Edema ; drug therapy ; etiology ; Brain Injuries, Traumatic ; complications ; drug therapy ; Gene Expression Regulation, Enzymologic ; drug effects ; Indazoles ; pharmacology ; therapeutic use ; MAP Kinase Signaling System ; drug effects ; Matrix Metalloproteinase 9 ; genetics ; Piperazines ; pharmacology ; therapeutic use ; Protein Kinase Inhibitors ; pharmacology ; therapeutic use ; Random Allocation ; Rats ; Rats, Sprague-Dawley

Objective To discuss the activation characteristics of the prefrontal cortex of people with mild cognitive impairment （MCI） due to brain trauma during working memory tasks. Methods The psychological experiment design software E-prime was used and N-back paradigm was adopted as working memory task. Functional near-infrared spectroscopy （fNIRS） was used to detect changes in cortical oxygenated hemoglobin concentrations of 22 channels within the prefrontal lobe of 24 people with MCI due to brain trauma （study group） and 27 healthy volunteers （control group） with matching gender and age. Behavioral data, such as the number of keystroke errors and reaction time, were recorded simultaneously. Independent samples t test and non-parametric test were used to compare the mean value of oxygenated hemoglobin concentration change, the number of key errors and the mean value of reaction time of the two groups in each task. Results （1） The differences in the number of errors and reaction time between the two groups in 1-back and 2-back tasks had statistical significance （P<0.05）.The main effects of task load and group were both significant （task F=14.11, P=0.001 1; group F=10.39, P=0.001 5）. （2） During the 1-back task, the differences in oxygenated hemoglobin concentration changes of the 22 channels between the two groups had no statistical significance （P>0.05）. During the 2-back task, the differences in oxygenated hemoglobin concentration changes of the two groups in channel 2, 3, 7, 9, 10, 11, 14, 15, 18, 19, 21 and 22 had statistical significance （P<0.05）. （3） In the 1-back task, the left frontal pole and dorsolateral prefrontal area in both groups were activated. In the 2-back task, the activation areas of the control group were the left frontal pole area and the left dorsolateral prefrontal area, while that of the study group almost covered most of the left and right frontal pole areas, which were scattered and the right area was activated, too. Conclusion Patients with MCI due to brain trauma have obvious working memory impairment, and during the 2-back working memory task, the activation of the prefrontal lobe decreased, but the activation range was wider.
Brain Injuries, Traumatic/complications* ; Cognitive Dysfunction/etiology* ; Humans ; Memory, Short-Term ; Prefrontal Cortex ; Spectroscopy, Near-Infrared

Objective To explore the impulse control and event-related potential （ERP） characteristics of patients with mental disorders caused by traumatic brain injury （TBI） in forensic psychiatry identification and to provide objective auxiliary indicators for forensic psychiatry identification. Methods Thirty patients （TBI group） with mental disorders caused by traumatic brain injury, who were identified as mild psychiatric impairment by judicial psychiatry, including 24 males and 6 females, as well as the thirty people in the control group participated in the study. All the participants completed Barratt Impulsiveness Scale-11 （BIS-11） and ERP induced by Go/NoGo tasks. BIS-11 and ERP data were collected and analyzed. Results The results of the BIS-11 showed that the total score and subscale scores of the TBI group were higher compared to the control group （P<0.05）. Moreover, the TBI group exhibited significantly lower NoGo-N2 amplitude and lower NoGo-P3 amplitude than the control group. The NoGo-N2 amplitude was larger than the Go-N2 amplitude, and the NoGo-P3 amplitude was larger than the Go-P3 amplitude in both groups （P<0.05）. Conclusion Traumatic brain injury could impair impulse control of mild psychiatric impairment patients, and the amplitudes of NoGo-N2 and NoGo-P3 could be important parameters to evaluate the impulse control of patients with mental disorders caused by traumatic brain injury.
Brain Injuries, Traumatic/complications* ; Electroencephalography ; Evoked Potentials ; Female ; Humans ; Inhibition, Psychological ; Male ; Mental Disorders/physiopathology* ; Neuropsychological Tests ; Reaction Time

Objective To explore the applied value of mismatch negative （MMN） in evaluation of severity of mental disorders due to traumatic brain injury. Methods Thirty-five patients（case group） that conform to the diagnostic criteria of organic （traumatic brain injury） mental disorder in ICD-10 Classification of Mental and Behavioural Disorders criteria were selected. Twenty-four healthy subjects （normal control group） that matched the case group in terms of gender, age composition ratio and educational level were selected. All subjects were evaluated by Activity of Daily Living Scale （ADL） and Social Disability Screening Schedule （SDSS） and then examined by Event-Related Potential （ERP）. A statistical analysis of the data was made by SPSS 22.0 software. Results The 32 patients and 24 normal control subjects completed the study. The scores of ADL and SDSS were significantly higher in the case group than in the normal control group （P<0.05）. The latency of Fz, FCz, Cz and Pz in the case group was significantly longer than that in the normal control group （P<0.05）. In the case group, the latency of Fz, FCz, Cz and Pz was positively correlated with the scores of ADL and SDSS （P<0.05）. The equation can be well fitted with the scores of ADL and SDSS. The latency and amplitude of Fz, FCz, Cz and Pz were used as concomitant variables and whether or not the subjects had mental disorders due to traumatic brain injury as dependent variables. Conclusion The latency of MMN can be used as an indicator in potential evaluation of the severity of mental disorders due to traumatic brain injury, which means that the longer the latency of MMN is, the more severe mental disorders due to traumatic brain injury may be. The combined application of ADL, SDSS and MMN can be an objective indicator in preliminary judgment of mental disorders due to traumatic brain injury.
Activities of Daily Living ; Brain Injuries, Traumatic/complications* ; Disabled Persons ; Evoked Potentials ; Humans ; Mental Disorders/etiology* ; Software ; Trauma Severity Indices

Traumatic brain injury (TBI) remains a major cause of death and disability worldwide. Increasing evidence indicates that TBI is an important risk factor for neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and chronic traumatic encephalopathy. Despite improved supportive and rehabilitative care of TBI patients, unfortunately, all late phase clinical trials in TBI have yet to yield a safe and effective neuroprotective treatment. The disappointing clinical trials may be attributed to variability in treatment approaches and heterogeneity of the population of TBI patients as well as a race against time to prevent or reduce inexorable cell death. TBI is not just an acute event but a chronic disease. Among many mechanisms involved in secondary injury after TBI, emerging preclinical studies indicate that posttraumatic prolonged and progressive neuroinflammation is associated with neurodegeneration which may be treatable long after the initiating brain injury. This review provides an overview of recent understanding of neuroinflammation in TBI and preclinical cell-based therapies that target neuroinflammation and promote functional recovery after TBI.
Age Factors ; Animals ; Brain ; immunology ; Brain Injuries, Traumatic ; complications ; therapy ; Cell- and Tissue-Based Therapy ; methods ; Exosomes ; Extracellular Vesicles ; physiology ; Female ; Humans ; Inflammation ; etiology ; Lymphatic System ; physiology ; Male ; Neuroprotective Agents ; Sex Characteristics

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

Persistent vegetative state (PVS) is a clinical condition wherein the cerebral cortex loses its function although brain stem function remains relatively intact. It has high mortality and disability rates. Although treatment for PVS is extensively studied in developed countries, little breakthrough has been made. In China, many PVS patients who were treated with traditional Chinese medicine (TCM) and acupuncture therapy were reported to have regained consciousness. In our department, we have been investigating TCM diagnosis and treatment methods for PVS for many years and have summarized a set of curative programs. Our patient is a male and 5 years and 3 months of age. He had traumatic brain injury and had been unconscious for three months on admission. Considering his condition, we adopted Xingnao Kaiqiao acupuncture, oral Angong Niuhuang Wan, and Xingnaojing intravenous drip. After the 50-day treatment, his health significantly improved and is nearly similar to that of a healthy child, indicating that the treatment is effective for PVS. Therefore, we decided to report the case and treatment methods.
Acupuncture Therapy ; methods ; Biological Products ; Brain Injuries, Traumatic ; complications ; Child, Preschool ; China ; Drugs, Chinese Herbal ; administration & dosage ; Humans ; Male ; Medicine, Chinese Traditional ; methods ; Persistent Vegetative State ; therapy ; Treatment Outcome

PURPOSEDespite the prevalence and cost of traumatic brain injury related disabilities, there is paucity in the literature on modern approaches to pharmacotherapy. Medications may promote recovery by enhancing some neurological functions without impacting others. Herein we discussed the role of bromocriptine in neurorehabilitation for patients with traumatic brain injury.

METHODSA cohort comprising of 36 selective nonsurgical cases of traumatic brain injury in minimally conscious state were enrolled in the study. After hemodynamic stability, bromocriptine was given at paediatric dose of 3.75 mg/d and adult dose of 7.5 mg/d. It was administered through a naso-gastric (NG) feeding tube in the patients with minimally conscious state, then changed to oral route after proper swallowing and good gag reflex were ensured in the patient. The drug was slowly reduced over three weeks after neurological improvement in the patients. Positive result was determined by improved GCS score of 2 and motor power by at least 1 British Medical Council (BMC) motor score. Improvement of deficits was evaluated in terms of fluency of speech for aphasia, task switching, digit span double tasking and trail-making test for cognition and attention, and functional independence measure score for motor functioning and self-independence.

RESULTSAccelerated arousal was seen in 47.0% of cases (8/17) in 4-40 days. In 41.2% of cases (7/17), Glasgow outcome score (GOS) was improved to 4/5 in 90 days. Improvement in hemiparesis by at least 1 BMC score was seen in 55.6% of cases (5/9) in 40 days. Aphasia was improved in 80% of cases (4/5) in 7-30 days. Moderate improvement in cognitive impairment was seen in 66.7% of cases (2/3) in 14-20 days. Improvement in memory was observed in 50% of cases (1/2) in over 30 days. No cases were withdrawn from the study because of adverse reactions of the drug. There was no mortality in the study group.

CONCLUSIONBromocriptine improves neurological sequelae of traumatic brain injury as well as the overall outcome in the patients. If medication is given to promote recovery and treat its associated disabilities, clinicians should thoroughly outline the goals and closely monitor adverse effects.

Adult ; Brain Injuries, Traumatic ; complications ; drug therapy ; Bromocriptine ; adverse effects ; therapeutic use ; Child ; Cohort Studies ; Glasgow Coma Scale ; Humans ; Morbidity ; Trauma Severity Indices