脑创伤患者急性期皮质醇分泌的变化

目的 探讨脑创伤患者急性期皮质醇(COR)分泌的变化.方法 创伤后2～24 h入院的脑创伤患者75例,根据Glasgow昏迷评分分为轻度脑创伤组(TBI1组,n=30)、中度脑创伤组(TBI2组,n=12)和重度脑创伤组(TBI3组,n=33),13例同期住院的颈椎病或颅骨骨瘤患者为对照组(C组).于入院后1 d时采集静脉血样,测定血清总COR、促肾上腺皮质激素和皮质醇结合球蛋白的浓度,计算游离COR浓度及游离COR指数.记录高血COR的发生情况.结果 与C组比较,TBI1组、TBI2组和TBI3组血清总COR、促肾上腺皮质激素、游离COR的浓度及游离COR指数均升高(P＜0.05),且TBI2组和TBI3组高于TBI1组(P＜0.05);四组间皮质醇结合球蛋白浓度比较差异无统计学意义(P＞0.05).TBI1组、TBI2组和TBI3组高血COR发生率高于C组,且TBI3组高于TBI1组和TBI2组(P＜0.05).结论 脑创伤患者急性期COR分泌升高,COR分泌水平与创伤程度有关.

Abstract：

Objective To investigate the changes in cortisol (COR) secretion in the acute phase of traumatic brain injury (TBI) .Method Seventy-five patients admitted to the hospital at 2-24 h after TBI were divided into 3 groups based on the Glasgow Coma Scale score: mild TBI group (group TBI1, n = 30), moderate TBI group (group TBI2, n = 12) and severe TBI group (TBI3, n = 33). Thirteen patients with cervical spondylosis or osteoma of the skull (admitted to the hospital at the same period) were regarded as control group (group C). Venous blood samples were taken on the first day after admission to measure the serum concentrations of total COR, adrenocorticotropin (ACTH) and corticosteroid-binding globulin (CBG). Free COR concentrations and free COR index were calculated. High blood COR was recorded. Result Compared with group C, the serum concentrations of total COR and ACTH, free COR levels and free COR index were significantly increased in TBI1, TBI2 and TBI3groups (P ＜ 0.05). The parameters mentioned above were significantly higher in TBI2 and TBI3 groups than in TBI1 group ( P ＜0.05). There was no significant difference in serum CBG concentrations among the four groups.The incidence of high blood COR was significantly higher in TBI1, TBI2 and TBI3 groups than in C group, and in TBI3 group thanin TBI1 and TBI2 groups (P ＜0.05). Conclusion COR secretion is increased in the acute phase of TBI and the level of COR secretion is related to the severity of brain damage.     

Analysis of US Veterans Health Administration comprehensive evaluations for traumatic brain injury in Operation Enduring Freedom and Operation Iraqi Freedom Veterans

Objective: To describe neurobehavioural symptoms in Iraq and Afghanistan war veterans evaluated for traumatic brain injury (TBI) through the Veterans Health Administration (VHA) TBI screening and evaluation programme. Design: An observational study based on VHA administrative data for all veterans who underwent TBI Comprehensive Evaluation between October 2007 and June 2010. Results: 55,070 predominantly white, non-Hispanic, male Veterans with a positive TBI screen had comprehensive TBI evaluations completed during the study period. Moderate-to-severe symptoms were common in the entire sample, both in those with and without a clinician-diagnosed TBI. However, the odds of reporting symptoms of this severity were significantly higher in those diagnosed with TBI compared to those without a TBI diagnosis, with odds ratios ranging from 1.35-2.21. TBI-specialty clinicians believed that in the majority of diagnosed TBI cases both behavioural health conditions and TBI contributed to patients' symptom presentation. Conclusions: The VHAs TBI screening and evaluation process is identifying individuals with ongoing neurobehavioural symptoms. Moderate-to-severe symptoms were more prevalent in veterans with TBI-specialty clinician determined TBI. However, the high rate of symptom reporting also present in individuals without a confirmed TBI suggest that symptom aetiology may be multi-factorial in nature.     

The reliability and validity of the SF-36 health survey questionnaire for use with individuals with traumatic brain injury

In order to examine the reliability and validity of the SF-36 for use with individuals with TBI, the SF-36 and three measures of health-related problems in persons with TBI (BDI-II, TIRR Symptom Checklist, Health Problems List) were administered to 271 individuals without a disability, 98 individuals with mild TBI, and 228 individuals with moderate-severe TBI. Internal consistency (reliability) was demonstrated for all SF-36 scales. Significant correlations were found between the SF-36 scales and the other measures, with stronger correlations emerging in the TBI groups. The TBI groups obtained significantly lower SF-36 scores than the comparison group, and the mild TBI group scored lower than the moderate-severe group. For the most part, the differences between the TBI groups disappeared when BDI-II scores were controlled for. These findings suggest that the SF-36 is a reliable and valid measure for use with persons with TBI.     

Secondary neurologic injury resulting from nonhypotensive hemorrhage combined with mild traumatic brain injury.

Although the emergency physician often treats patients with multiple injuries, there are relatively few clinically relevant models that mimic these situations. To describe the changes after a hemorrhagic insult superimposed on traumatic brain injury (TBI), anesthetized and ventilated juvenile pigs were assigned to 35% hemorrhage (35H), TBI (via fluid percussion); TBI + 35H, and TBI + 40H (40% hemorrhage). Animals were resuscitated with shed blood and crystalloid. Hemodynamic, metabolic, behavioral, and histologic parameters were assessed for 48 h. In TBI, mean arterial pressure (MAP) was not significantly different from baseline. For TBI + 40H, MAP fell by 60% (p < 0.05). This was corrected with resuscitation. Interestingly, TBI + 35H did not show a fall in MAP, while in 35H, MAP was reduced similarly to the TBI + 40H group. ICP was elevated only initially in the TBI group. In TBI + 40H and TBI + 35H, ICP increased markedly with resuscitation, remaining elevated for 60 min. ICP remained at baseline with 35 H. Hemorrhagic focal cerebal contusions at the gray-white interface were observed in 3/5 of TBI + 40H and 5/7 of TBI + 35H. Despite the presence of subarachnoid hemorrhage (SAH) in all the animals in the TBI alone group, none of these animals demonstrated grossly discernible intraparenchymal injury. There was no evidence of intracranial injury in the 35H group. Only in animals receiving a secondary insult of hemorrhage following the primary TBI were cerebral contusions found. These experiments demonstrate the evolution of cerebral contusions as a form of secondary neurologic injury following resuscitation from traumatic brain injury and hemorrhage, even in the absence of significant blood pressure changes.     

Head injury mortality in the Nordic countries

Traumatic brain injury (TBI) is a major cause of morbidity and mortality in Western countries. Effective management planning for these patients requires knowledge of TBI epidemiology. The purpose of this study was to describe and analyze the development of TBI mortality in the Nordic countries during the period 1987-2001. Data on TBI deaths were retrieved from the national official statistical agencies according to specified diagnostic codes. We also collected data on the number of operations for acute TBI in the year 2000 from all Nordic hospitals admitting trauma patients. Finland had about twice as high a TBI mortality rate as the other countries. Similarly, the Finnish incidence of acute TBI operations was nearly twice that of the other countries. The median TBI death rate for Finland was 21.2 per 100,000 per year, and for Denmark, Norway, and Sweden 11.5, 10.4, and 9.5, respectively. There were more male than female deaths in all countries. The mortality rate from extracranial injuries was relatively equal between the countries. We observed a sizeable reduction in TBI mortality rates for all countries, except in Finland. Younger age groups had the most pronounced decrease in TBI mortality rates. The oldest age group had the least favorable development of TBI mortality rates, and the mean age of TBI casualties increased substantially during the study period. This study demonstrates considerable differences in and between the Nordic countries regarding TBI mortality. Preventive measures and implementation of regional guidelines are needed to assure a positive development in the future.     

Prevalence of traumatic brain injury in psychiatric and non-psychiatric subjects

Traumatic brain injury (TBI) and its sequelae may impact the expression and treatment of psychiatric disorders. The prevalence of TBI in psychiatric patients is unknown and investigations in the general population are limited. This study examined the prevalence of TBI with loss of consciousness in mental health setting patients (n = 231), general hospital and university staff and students (n = 534) and non-psychiatric medical clinical patients (n = 59). The Traumatic Brain Injury Questionnaire was used to assess TBI. A greater percentage of psychiatric patients reported TBI than medical patients or staff and students. Traumatic brain injuries were typically mild-moderate, medical assistance was frequently sought and use of alcohol and drugs was reported in a minority of TBI incidents. Multiple injuries were most common in psychiatric patients. The percentage of medical patients and staff and students reporting TBI was similar to previous research. The greater percentage of psychiatric patients reporting TBI indicates the need to assess TBI in this population. The role of TBI in the emergence, expression and treatment outcome of psychiatric disorders and the risk factors that leave psychiatric patients vulnerable to TBI should be further examined.     

Traumatic brain injury, alcohol and quantitative neuroimaging: preliminary findings

Magnetic resonance (MR) quantitative neuroimaging analysis was undertaken with a large group of normal (n = 197) and traumatically brain injured (TBI, n = 99) adults. Of the TBI subjects 18 patients were identified with a history of substance-related abuse (TBI/Abuse group). Both the TBI/Abuse group and the remaining sample of TBI patients ( n = 81, TBI/Non-abuse group) without a history of substance-related abuse differed significantly from the control group on most quantitative MRimaging analyses. The TBI/Abuse group displayed the greatest degree of atrophic change. However, the TBI/ Abuse group had a significantly lower Glasgow Coma Scale (GCS) score, ostensibly suggesting that those with substance-related abuse suffered more severe brain injury than non-abuse TBI patients. When a subset (n = 18) of the TBI/Non-abuse group was matched by GCS, gender and age to the TBI/Abuse group, both groups differed significantly from the control group on most morphometric measures, but did not differ from one another. Results are discussed in terms of the potential adverse role that substance-related abuse, particularly alcohol, plays in the individual who sustains traumatic injury to the brain.     

Hypoxia alters the expression of inhibitor of apoptosis proteins after brain trauma in the mouse

Hypoxia worsens brain injury following trauma, but the mechanisms remain unclear. The purpose of this study was to determine the effect of traumatic brain injury (TBI) and secondary hypoxia (9% oxygen) on apoptosis-related protein expression, cell death, and behavior. Using a murine weight-drop model, TBI led to an early (6 h) increase followed by a later (24 h) decrease in neuronal apoptosis inhibitor protein (NAIP) expression in the olfactory and motor cortex; in contrast, TBI led to a sustained (6 h to 7 days) increase in NAIP in the striatum. The peak increase in the expression of NAIP (6-12 h) following TBI alone was delayed (1-7 days) when hypoxia was added to TBI. Hypoxia following TBI further depleted other apoptosis inhibitor proteins (IAPs) and activated caspases, as well as increased contusion size and worsened cell death. Hypoxia added to TBI also increased motor and feeding activity on days 2 and 4 compared to TBI alone. Hypoxia without TBI had no effect on the expression of IAPs or cell death. These findings show that IAPs have a potential role in the increased vulnerability of brain cells to hypoxia following TBI, and have implications for configuring future therapies for TBI.     

Improving identification of traumatic brain injury after nonmilitary bomb blasts

OBJECTIVE: To improve identification of traumatic brain injury (TBI) in survivors of nonmilitary bomb blasts during the acute care phase. METHODS: The Centers for Disease Control and Prevention convened a meeting of experts in TBI, emergency medicine, and disaster response to review the recent literature and make recommendations. RESULTS: Seven key recommendations were proposed: (1) increase TBI awareness among medical professionals; (2) encourage use of standard definitions and consistent terminology; (3) improve screening methods for TBI in the acute care setting; (4) clarify the distinction between TBI and acute stress disorder; (5) encourage routine screening of hospitalized trauma patients for TBI; (6) improve identification of nonhospitalized TBI patients; and (7) integrate the appropriate level of TBI identification into all-hazards mass casualty preparedness. CONCLUSIONS: By adopting these recommendations, the United States could be better prepared to identify and respond to TBI following future bombing events.     

Mercaptoethylguanidine inhibition of inducible nitric oxide synthase and cyclooxygenase-2 expressions induced in rats after fluid-percussion brain injury

The present study examined the temporal expression of nitric oxide synthase (iNOS) and cyclo-oxygenase (COX)-2 in rat brains after traumatic brain injury (TBI). We studied the effects of mercaptoethylguanidine (MEG), a dual inhibitor of the inducible iNOS and COX with scavenging effect on peroxynitrite, on physiologic variables, brain pathogenesis, and neurologic performance in rats after a lateral fluid percussive-induced TBI. Mean arterial blood pressure and percentage cerebral tissue perfusion in MEG-treated TBI rats showed significant improvement when compared with TBI rats. Immunohistochemical analysis showed a marked number of iNOS and COX-2 immunopositive cells in the cerebral cortex ipsilateral to the injury in TBI rats when compared with MEG-treated TBI rats. MEG also significantly decreased the number of hyperchromatic and shrunken cortical neurons when compared with TBI rats' brain nitrate/nitrite, and prostaglandin E2 levels were attenuated in MEG-treated TBI rats when compared with TBI rats. It is therefore suggested that treatment of MEG via inhibition of iNOS and COX-2 might contribute to improved physiologic variables, neuronal cell survival, and neurologic outcome after TBI.     

Classification of the Spectrum of Mild Traumatic Brain Injury

Mild traumatic brain injury (TBI) is a very common injury, resulting in immediate and possible long-term symptoms. The accurate and consistent definition of mild TBI is important in the initial and rehabilitation management of the injury, and in research concerning mild TBI. A definition of mild TBI has been developed by the Head Injury Interdisciplinary Special Interest Group of the American Congress of Rehabilitation Medicine. Within the spectrum of injury severity in mild TBI there are several classification systems, primarily used in management of acute mild TBI, that breakdown mild TBI into grades of injury severity. These are based upon the presence or absence of mental status changes, amnesia, loss of consciousness, anatomical lesion or neurological deficit.     

Social and behavioural effects of traumatic brain injury in children

Traumatic brain injury (TBI) is the leading cause of death and permanent disability in children and adolescents. Although cognitive and behavioural effects have now been reported for all degrees of TBI severity in children, other aspects of functioning which might be related (such as psychosocial adjustment), have been neglected. In the present study the social and behavioural effects of TBI were assessed by comparing 27 TBI children with 27 controls. TBI children demonstrated significantly lower levels of self esteem and adaptive behaviour, and higher levels of loneliness, maladaptive behaviour and aggressive/antisocial behaviour. These findings confirm the previously demonstrated detrimental effects of TBI on children s behavioural functioning and offer new evidence for the detrimental effects of TBI on children s social functioning.     

The sensitivity and specificity of self-reported symptoms in individuals with traumatic brain injury

In this study, self-reported symptoms (cognitive, physical, behavioural/affective) from the TIRR Symptom Checklist are compared across six panels: 135 individuals with mild TBI, 275 with moderate/severe TBI, 287 with no disability, 104 with spinal cord injury, 197 who are HIV positive and 107 who had undergone liver transplantation. Participants with TBI and SCI were at least 1 year postinjury. Individuals with TBI reported significantly more symptoms than other panels. Symptom reports in the TBI panels were independent of demographic variables (gender, education, income, ethnicity, age), as well as time since injury and depression. Five of the 67 symptoms were found to be sensitive/specific to TBI in general; 25 symptoms were sensitive/specific to mild TBI (23 were cognitive, one physical and one behavioural/affective). Implications of these results in terms of current debates about the 'reality' of symptom reports in individuals with mild TBI are discussed, as well as implications for using symptom checklists for TBI screening.     

Use of the Beck Depression Inventory-II (BDI-II) with persons with traumatic brain injury: analysis of factorial structure

PRIMARY OBJECTIVE: To determine the factorial structure of the BDI-II in a TBI sample and possible predictor variables of depression following TBI. RESEARCH DESIGN: Principle components analysis with orthogonal rotation and linear regression analyses. METHODS AND PROCEDURES: Fifty-one individuals with traumatic brain injury (TBI) participated in this study. The factorial structure of the BDI-II, a 21-item self-report measure of depression, was examined with individuals in the early stages following TBI. Time since injury, severity of injury, location of lesion and previous substance abuse were examined as possible predictors of depression following TBI. RESULTS: A three-factor structure of the BDI-II was found for the TBI sample, which included Negative Self-Evaluation, Symptoms of Depression and Vegetative Symptoms of Depression. Time since injury was the only significant predictor of depression following TBI. CONCLUSION: Using the BDI-II, symptoms of depression after TBI fall into three key categories. With time since injury being the only significant predictor of depression following TBI, it appears that the depression could be more of a result of psychosocial factors than neurobiological factors. It was concluded that BDI-II can be useful in identifying symptoms of depression in the early stages following TBI.     

Effect of leptin on bone metabolism in rat model of traumatic brain injury and femoral fracture

Objective: To observe serum and callus leptin expression within the setting of fracture and traumatic brain injury (TBI).Methods: Atotal of 64 male SD rats were randomized equally into 4 groups: nonoperated group, TBI group, fraeture group, and fracture+TBI group. Rats were sacrificed at 2, 4, 8 and 12 weeks after fracture+TBI. Serum leptin was detected using radioimmunoassay, and callus formation was measured radiologically. Callus leptin was analyzed by immunohistochemistry.Results: Serum ieptin levels in the fracture group, TBI group and combined fracture+TBI group were all significantly increased compared with control group at the 2 week time-point (P＜0.05). Serum leptin in the combined fracture +TBI group was significantly higher than that in the fracture and TBI groups at 4 and 8 weeks after injury (P＜0. 05).The percentage of leptin-positive cells in the fracture+TBI callus and callus volume were significantly higher than those in the fracture-only group (P＜0.01).Conclusions: We demonstrated elevated leptin expression within healing bone especially in the first 8 weeks in a rat model of fracture and TBI. A close association exists between leptin levels and the degree of callus formation in fractures.     

Traumatic brain injury in a county jail population: prevalence,neuropsychological functioning and psychiatric disorders

Primary objective : To determine the prevalence of traumatic brain injury (TBI) among inmates in a county jail population.

Research design : Cross-sectional, observational study.

Methods and procedures : A standardized interview was used to determine prevalence of TBI in 69 randomly selected inmates. To examine cognitive and emotional differences between subjects with and without recent TBI, neuropsychological tests and structured psychiatric diagnostic interviews were conducted with 50 subjects (the first 25 with TBI and the first 25 without TBI in the prior year).

Results : Sixty (87.0%) reported TBI over their lifetime; 25 (36.2%) reported TBI in the prior year. The latter group had significantly worse anger and aggression scores and had a trend towards poorer cognitive test results and a higher prevalence of psychiatric disorders than the group without TBI in the prior year.

Conclusion : This study suggests the need for increased attention to TBI and its cognitive, behavioural and psychiatric sequelae in jail populations.     

Comparison of nursing home residents with and without traumatic brain injury: use of the Minimum Data Set

OBJECTIVE: To describe the magnitude of the population with traumatic brain injury (TBI) in Colorado living in nursing homes and compare these residents to the nursing home residents with neither TBI nor dementia. METHODS: The standardized Minimum Data Set of resident assessments was used to describe the behavior, cognitive performance, activities of daily living, and discharge potential of residents. RESULTS: There were 16,478 nursing home residents in 2005, of whom 1.4% had TBI but not dementia, 0.7% had both TBI and dementia, and 50.2% had neither diagnosis. The prevalence of TBI in this population was 2.1%. TBI residents without dementia were younger (median age 53 years). A larger proportion consisted of men (64%), from a racial/ethnic minority (24%), and needed greater assistance with eating, toileting, and hygiene. The percent with severe cognitive impairment was greater for individuals with TBI (22%) compared to those with neither TBI nor dementia (5%). Fewer TBI residents expressed a preference to return to the community. CONCLUSION: These differences suggest the need for increased training and staffing to care for nursing home residents with TBI.     

Posttraumatic Stress Disorder is a Stronger Predictor of Long-Term Neurobehavioral Outcomes Than Traumatic Brain Injury Severity

Concurrent posttraumatic stress disorder (PTSD) and traumatic brain injury (TBI) is common in military populations. The purpose of this study was to examine long-term neurobehavioral outcomes in service members and veterans (SMVs) with versus without PTSD symptoms following TBI of all severities. Participants were 536 SMVs prospectively enrolled from three military medical treatment facilities who were recruited into three experimental groups: TBI, injured controls (IC), and noninjured controls (NIC). Participants completed the PTSD Checklist, Neurobehavioral Symptom Inventory, and the TBI–Quality of Life (TBI-QOL) and were divided into six subgroups based on the three experimental categories, two PTSD categories (i.e., present vs. absent), and two broad TBI severity categories (unMTBI, which included uncomplicated mild TBI; and smcTBI, which included severe TBI, moderate TBI, and complicated mild TBI): (a) NIC/PTSD-absent, (b) IC/PTSD-absent, (c) unMTBI/PTSD-absent, (d) unMTBI/PTSD-present, (e) smcTBI/PTSD-absent, and (f) smcTBI/PTSD-present. There were significant main effects across the six groups for all TBI-QOL measures, ps < .001. Select pairwise comparisons revealed significantly lower scores, p < .001, on all TBI-QOL measures in the PTSD-present groups when compared to the PTSD-absent groups within the same TBI severity classification, ds = 0.90–2.11. In contrast, when controlling for PTSD, there were no significant differences among the TBI severity groups for any TBI-QOL measures. These results provide support for the strong influence of PTSD but not TBI severity on neurobehavioral outcomes following TBI. Concurrent PTSD and TBI of all severities should be considered a risk factor for poor long-term neurobehavioral outcomes that require ongoing monitoring.     

Current understanding of neuroinflammation after traumatic brain injury and cell-based therapeutic opportunities

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.