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

Brain Concussion ; complications ; Hearing ; Hearing Disorders ; prevention & control ; Humans ; Thioctic Acid ; therapeutic use

OBJECTIVE: To investigate the different kinds of controversial cases of mental disability after brain damage, to analysis the problems in the first appraisal, and to explore solutions of the problems. METHODS: The reappraisals of mental disorders after traumatic brain damage were collected from 2007-2011 in Shanghai forensic center, and the first appraisal and reappraisal cases were analyzed and compared. RESULTS: The changes of conclusion in reappraisal cases showed the following major reasons: inappropriate appraisal time, not comprehensive and object investigation of mental state of patients in first appraisal, misunderstanding the standards, etc. CONCLUSION The quality improvement of appraisal should adopt the following measures: regulating the practice, improvement of the professional skills of experts, choosing appropriate appraisal time, improvement of appraisal standards, etc.
Accidents, Traffic ; Activities of Daily Living ; Adolescent ; Adult ; Aged ; Brain Concussion/diagnosis* ; Brain Injuries/complications* ; Child ; Disability Evaluation ; Female ; Forensic Psychiatry ; Humans ; Intellectual Disability/psychology* ; Male ; Mental Disorders/psychology* ; Middle Aged ; Retrospective Studies ; Severity of Illness Index ; Time Factors ; Young Adult

OBJECTIVE: To observe the change of c-fos protein(Fos) and nerve growth factor receptor (NGFR) staining in the brain of rat after experimental brain contusion. METHODS: Immunohistochemistry of c-fos and NGFR were applied to investigate the brain contusion. RESULTS: (1) The expression of Fos protein could be observed at 0.5 h after injury and then increased with the prolonging of time. By 3 h after injury, the positive staining cells could be detected massively not only in and round the wound site but also in other areas of the whole ipsilateral cortex. The stains decreased 6-12 h later and could hardly be detected 1 d after the brain contusion. The control-experiment is negative. (2) NGFR positive staining cells could be found round the wound area 1 d postlesion. At 3 d following injury, a peak of massive positively stained cells appeared both in number and in intensity, showing significant differences compare with that of 1 d after damage (P < 0.01). 5 d later the positive express declined slowly. The express in the control-rat is negative. CONCLUSION There is a rule that the expression of Fos and NGFR positive staining changes with time going after brain contusion, which will be of great value in estimation of brain injury time. Detection of Fos can be used for time deduction in earlier period after injury, while NGFR in later period. They are also very important for distinguishing between antemortem or postmortem injury.
Animals ; Brain Concussion/complications* ; Brain Injuries/pathology* ; Female ; Immunohistochemistry ; Male ; Neuroglia/metabolism* ; Neurons/metabolism* ; Proto-Oncogene Proteins c-fos/metabolism* ; Rats ; Rats, Wistar ; Receptor, Nerve Growth Factor/metabolism* ; Time Factors

OBJECTIVETo discuss the mechanism of cerebral vessel spasm caused by concussion and the effect of Nimodipine on concussion.

METHODSA total of 224 patients who were treated from March 1995 to October 1999 were divided into two groups randomly, ie, Nimodipine group (113 cases) and control group (111 cases). Middle cerebral artery (MCA), basilar artery (BA) and the average peak forward velocity of cerebral blood flow were observed by color three-dimensional transcranial Doppler (3D-TCD) within 24 hours after admission and at the end of 3-6 days of treatment. Cerebral blood flow changes, characteristics and treatment effect were analyzed and determined by clinical main symptom disappearance rate.

RESULTSIn concussion, cerebral blood flow was divided into 3 phases: cerebral blood flow low infusion dilation phase, cerebral blood vessel spasm phase and cerebral blood flow recovery phase. In the Nimodipine group, clinical main symptom disappearance rate was higher than that in the control group in the cerebral spasm and recovery phases with a significant difference (P < 0.01).

CONCLUSIONSCerebral vessel spasm, hypoxia and ischemia lesion are the main pathological changes. Whether cerebral dysfunction is reversible or not is mainly determined by spasm time of cerebral blood vessel. Nimodipine has a good effect on releasing spasm and diminishing the cerebral blood flow velocity. It not only improves curative effect on concussion, but also reduces and prevents concussion sequelae. Hence, concussion patients who have cerebral spasm confirmed by 3D-TCD should be given Nimodipine routinely and early.

Adolescent ; Adult ; Aged ; Blood Flow Velocity ; Brain Concussion ; complications ; diagnostic imaging ; Cerebral Arteries ; diagnostic imaging ; drug effects ; Cerebrovascular Circulation ; drug effects ; Dose-Response Relationship, Drug ; Drug Administration Schedule ; Drug Therapy, Combination ; Female ; Follow-Up Studies ; Humans ; Infusions, Intravenous ; Injury Severity Score ; Male ; Mannitol ; administration & dosage ; Middle Aged ; Nimodipine ; administration & dosage ; Reference Values ; Treatment Outcome ; Ultrasonography, Doppler, Transcranial ; Vasospasm, Intracranial ; drug therapy ; etiology ; physiopathology