Significant other burden and factors related to it in traumatic brain injury

Feelings of burden and factors related to it were examined in a sample of 180 relatives of moderately to severely traumatically brain injured (TBI) subjects 6 months postinjury. Relatives were enrolled onto the study based on their family member's head injury and not on outcome. The results indicate that although both positive and negative experiences were common, the majority of the relatives reported an overall positive experience. The significant other's (SO's) experience was significantly and systematically related to many factors with overall negative experience associated with increased brain injury severity, worse neuropsychological functioning, increased dependency on others, SO's report of changes in the TBI subject, changes in the SO's life as a result of caregiving and SO depression.     

Patients' and relatives' experience of difficulties following severe traumatic brain injury: The sub-acute stage

The present study aimed to (1) identify the difficulties most frequently reported by individuals with severe traumatic brain injury (TBI) at the time of discharge from a sub-acute rehabilitation brain injury unit as well as difficulties reported by their relatives, (2) compare patients' and relatives' reports of patient difficulties, and (3) explore the role of injury severity, disability and other factors on subjective experience of difficulties. The primary measure was the European Brain Injury Questionnaire (EBIQ) administered to patients and to one of their close relatives at discharge. Results from 52 patients and 50 relatives indicate that the most frequent complaints in both groups related to somatic and cognitive problems. Relatives reported significantly more difficulties than patients on all subscales of the EBIQ. However, the level of complaints in both patients and relatives was low compared to other studies using the EBIQ. Furthermore, the effects of injury severity and general level of functioning had limited impact on the subjective experience of difficulties. Implications of these findings, specifically as they pertain to the sub-acute stage are discussed.     

Awareness of behavioral limitations after traumatic brain injury: A cross-cultural study of New Zealand maoris and non-maoris

Forty-one New Zealand traumatic brain injury (TBI) patients were studied using the Patient Competency Rating Scale (PCRS) and selected neuropsychological tests. An attempt was made to replicate earlier reported findings in American TBI patients and determine if cultural factors influence self-perceptions (i.e., awareness) of impairments after brain injury. TBI patients with Maori ancestry were compared to New Zealanders with non-Maori (English) ancestry. Both groups showed no correlation between their actual neuropsychological status and self-reports of behavioral competency. In contrast, the ratings of their relatives concerning their behavioral competency were correlated with the patient's neuropsychological test performance. Maori TBI patients reported less behavioral competency than non-Maori TBI patients. Non-Maori TBI patients' performance on the PCRS replicated the findings obtained with American TBI patients. An earlier finding of slow speed of left-hand finger tapping in patients who overestimate their behavioral competency was not replicated, but a confounding of ethnicity and finger-tapping speed was observed. Brain damage may contribute to patients' misperceptions of their behavioral competency, but cultural factors also seem to play an important role.     

Patients' and relatives' experience of difficulties following severe traumatic brain injury: the sub-acute stage

The present study aimed to (1) identify the difficulties most frequently reported by individuals with severe traumatic brain injury (TBI) at the time of discharge from a sub-acute rehabilitation brain injury unit as well as difficulties reported by their relatives, (2) compare patients' and relatives' reports of patient difficulties, and (3) explore the role of injury severity, disability and other factors on subjective experience of difficulties. The primary measure was the European Brain Injury Questionnaire (EBIQ) administered to patients and to one of their close relatives at discharge. Results from 52 patients and 50 relatives indicate that the most frequent complaints in both groups related to somatic and cognitive problems. Relatives reported significantly more difficulties than patients on all subscales of the EBIQ. However, the level of complaints in both patients and relatives was low compared to other studies using the EBIQ. Furthermore, the effects of injury severity and general level of functioning had limited impact on the subjective experience of difficulties. Implications of these findings, specifically as they pertain to the sub-acute stage are discussed.     

硫氧还蛋白还原酶 TrxR2在颅脑损伤大鼠皮质的表达变化

目的：探究硫氧还蛋白还原酶2（TrxR2）在颅脑损伤大鼠皮质的动态表达变化。方法54只雄性 SD 大鼠,随机分为正常对照组（n =6）和颅脑损伤组（n =48）。颅脑损伤组采用改良的 Freeny＆#39;s 自由落体装置制作颅脑损伤大鼠模型,正常对照组不做处理。伤后1 h、3 h、6 h、12 h、24 h、3 d、7 d、14 d,采用实时荧光定量 PCR （quantitative real-time PCR,qRT-PCR）和Western blot 检测挫伤区周围皮质 TrxR2 mRNA 和蛋白的表达变化情况。结果 qRT-PCR 结果显示：皮质中 TrxR2 mRNA 颅脑损伤后1 h 表达增加,24 h 达到高峰,7 d 恢复正常;颅脑损伤组伤后1 h~3 d 各时间点 TrxR2 mRNA 表达明显高于正常对照组（均 P ＜0.05）。Western blot 检测显示：TrxR2蛋白在颅脑损伤后1 h 表达增加,24 h 达到高峰,14 d 恢复正常;颅脑损伤组1 h~7 d 各时间点 TrxR2蛋白表达高于正常对照组（均 P ＜0.05）。结论颅脑损伤后 TrxR2表达增多,提示 TrxR2作为一种急性应激反应蛋白参与颅脑损伤早期抗氧化应激反应。     

颅脑损伤程度对大鼠脑血流及氧代谢的影响

目的 对颅脑损伤影响脑血流及氧代谢进行前瞻性研究。方法 30只Wistar大白鼠分成3组：颅脑损伤1组（TBI1）、2组（TBI2）及3组（TBI3）各10只,分别为轻、中、重型颅脑损伤。用脑阻抗（REG）测定脑血流量,颈内静脉血氧饱和度（SjVO2)反映全脑氧代谢情况。结果 TBI、TBI2及TBI3组影响脑血流和氧代谢程度依次为TBI3＞TBI2＞TBI1,健侧脑组织含水量各组无明显差异,伤侧脑组织含水量TBI3组最多,其次为TBI2,明显高于TBI1组（P＜0．01）。结论 颅脑损伤后脑血流和氧代谢变化取决于损伤程度,脑血流和氧代谢各参数的监测对正确认识脑组织病理生理变化,指导临床治疗,判断预后有重要价值。     

Traumatic brain injury and obesity induce persistent central insulin resistance

Traumatic brain injury (TBI)‐induced impairments in cerebral energy metabolism impede tissue repair and contribute to delayed functional recovery. Moreover, the transient alteration in brain glucose utilization corresponds to a period of increased vulnerability to the negative effects of a subsequent TBI. In order to better understand the factors contributing to TBI‐induced central metabolic dysfunction, we examined the effect of single and repeated TBIs on brain insulin signalling. Here we show that TBI induced acute brain insulin resistance, which resolved within 7 days following a single injury but persisted until 28 days following repeated injuries. Obesity, which causes brain insulin resistance and neuroinflammation, exacerbated the consequences of TBI. Obese mice that underwent a TBI exhibited a prolonged reduction of Akt (also known as protein kinase B) signalling, exacerbated neuroinflammation (microglial activation), learning and memory deficits, and anxiety‐like behaviours. Taken together, the transient changes in brain insulin sensitivity following TBI suggest a reduced capacity of the injured brain to respond to the neuroprotective and anti‐inflammatory actions of insulin and Akt signalling, and thus may be a contributing factor for the damaging neuroinflammation and long‐lasting deficits that occur following TBI.     

Altered resting‐state functional connectivity within the developing social brain after pediatric traumatic brain injury

Traumatic brain injury (TBI) in childhood and adolescence can interrupt expected development, compromise the integrity of the social brain network (SBN) and impact social skills. Yet, no study has investigated functional alterations of the SBN following pediatric TBI. This study explored functional connectivity within the SBN following TBI in two independent adolescent samples. First, 14 adolescents with mild complex, moderate or severe TBI and 16 typically developing controls (TDC) underwent resting‐state functional magnetic resonance imaging 12–24 months post‐injury. Region of interest analyses were conducted to compare the groups' functional connectivity using selected SBN seeds. Then, replicative analysis was performed in an independent sample of adolescents with similar characteristics (9 TBI, 9 TDC). Results were adjusted for age, sex, socioeconomic status and total gray matter volume, and corrected for multiple comparisons. Significant between‐group differences were detected for functional connectivity in the dorsomedial prefrontal cortex and left fusiform gyrus, and between the left fusiform gyrus and left superior frontal gyrus, indicating positive functional connectivity for the TBI group (negative for TDC). The replication study revealed group differences in the same direction between the left superior frontal gyrus and right fusiform gyrus. This study indicates that pediatric TBI may alter functional connectivity of the social brain. Frontal‐fusiform connectivity has previously been shown to support affect recognition and changes in the function of this network could relate to more effortful processing and broad social impairments.     

Neurorehabilitation and cognitive-behaviour therapy of anxiety disorders after brain injury: An overview and a case illustration of obsessive-compulsive disorder

Survivors of acquired and traumatic brain injuries may often experience anxiety states. Psychological reactions to neurological trauma may be caused by a complex interaction of a host of factors. We explore how anxiety states may be understood in terms of a biopsychosocial formulation of such factors. We also review the current evidence for the presence of specific anxiety disorders after brain injury. We then describe how cognitive-behaviour therapy (CBT), a treatment of choice for many anxiety disorders, may be integrated with cognitive rehabilitation (CR), for the management of anxiety disorders in brain injury. We illustrate how CBT and CR may be delivered with a case of a survivor of traumatic brain injury (TBI) who had developed obsessive compulsive disorder and health anxiety. We show how CBT plus CR allows a biopsychosocial formulation to be developed of the survivor's concerns for guiding a goal-based intervention. The survivor made significant gains from intervention in terms of goals achieved and changes on clinical measures. We argue that large-scale research is needed for developing an evidence base for managing emotional disorders in brain injury.     

The neuropsychiatry of depression after brain injury

Biological aspects of depression after brain injury, in particular traumatic brain injury (TBI) and stroke, are reviewed. Symptoms of depression after brain injury are found to be rather non-specific with no good evidence of a clear pattern distinguishing it from depression in those without brain injury. Nevertheless symptoms of disturbances of interest and concentration are particularly prevalent, and guilt is less evident. Variabilitiy of mood is characteristic. The prevalence of depression is similar after both stroke and TBI with the order of 20-40% affected at any point in time in the first year, and about 50% of people experience depression at some stage. There is no good evidence for areas of specific vulnerability in terms of lesion location, and early suggestions of a specific association with injury to the left hemisphere have not been confirmed. Insight appears to be related to depressed mood with studies of TBI indicating that greater insight over time post-injury may be associated with greater depression. We consider that this relationship may be due to depression appearing as people gain more awareness of their disability, but also suggest that changes in mood may result in altered awareness. The risk of suicide after TBI is reviewed. There appears to be about a three to fourfold increased risk of suicide after TBI, although much of this increased risk may be due to pre-injury factors in terms of the characteristics of people who suffer TBI. About 1% of people who have suffered TBI will commit suicide over a 15-year follow-up. Drug management of depression is reviewed. There is little specific evidence to guide the choice of antidepressant medication and most psychiatrists would start with a selective serotonin reuptake inhibitor (SSRI). It is important that the drug management of depression after brain injury is part of a full package of care that can address biological as well as psychosocial factors in management.     

Evaluation of coping resources and self-esteem as moderators of the relationship between threat appraisals and avoidance of activities after traumatic brain injury

It is not uncommon for people after a traumatic brain injury (TBI) to develop anxieties about possible negative outcomes (i.e., threat appraisals) in relation to participating in valued activities. Some respond to this anxiety by avoiding the activities, but others maintain their participation. The present study investigated two factors that may help explain this variation across individuals in their response to threat appraisals – self-esteem and the evaluation of coping resources. Forty-one individuals with a TBI completed the Avoidance and Threat Appraisals Questionnaire, the Rosenberg Self-Esteem Scale and the Coping Resources Questionnaire. The study's hypotheses were supported: Those low in self-esteem, and those with a negative evaluation of their ability to cope with the TBI, were significantly more likely to respond to threat appraisals with avoidance. Those whose injury was more recent and those whose injury was the result of an assault were also more likely to respond with avoidance. The theoretical and therapeutic implications of these results are discussed.     

The neuropsychiatry of depression after brain injury

Biological aspects of depression after brain injury, in particular traumatic brain injury (TBI) and stroke, are reviewed. Symptoms of depression after brain injury are found to be rather non-specific with no good evidence of a clear pattern distinguishing it from depression in those without brain injury. Nevertheless symptoms of disturbances of interest and concentration are particularly prevalent, and guilt is less evident. Variabilitiy of mood is characteristic. The prevalence of depression is similar after both stroke and TBI with the order of 20–40% affected at any point in time in the first year, and about 50% of people experience depression at some stage. There is no good evidence for areas of specific vulnerability in terms of lesion location, and early suggestions of a specific association with injury to the left hemisphere have not been confirmed. Insight appears to be related to depressed mood with studies of TBI indicating that greater insight over time post-injury may be associated with greater depression. We consider that this relationship may be due to depression appearing as people gain more awareness of their disability, but also suggest that changes in mood may result in altered awareness. The risk of suicide after TBI is reviewed. There appears to be about a three to fourfold increased risk of suicide after TBI, although much of this increased risk may be due to pre-injury factors in terms of the characteristics of people who suffer TBI. About 1% of people who have suffered TBI will commit suicide over a 15-year follow-up. Drug management of depression is reviewed. There is little specific evidence to guide the choice of antidepressant medication and most psychiatrists would start with a selective serotonin reuptake inhibitor (SSRI). It is important that the drug management of depression after brain injury is part of a full package of care that can address biological as well as psychosocial factors in management.     

Clinical epidemiology of posttraumatic epilepsy in a group of Chinese patients

ObjectiveTo explore the incidence, types of onset, and risk factors of posttraumatic epilepsy (PTE).MethodsThis is a retrospective follow-up study of patients discharged from the Affiliated Hospital of the Medical College of the Chinese People's Armed Police Forces between September 2004 and September 2008 with a diagnosis of traumatic brain injury (TBI).ResultsComplete clinical information was available on 2826 patients. Of the 2826 TBI patients, 141 developed PTE, providing an incidence rate of 5.0%. Twenty-four cases (0.8%) had posttraumatic seizures (PTS), of which 16 (66.7%) continued to experience after the acute phase of their TBI, accounting for 5.0% of the total PTE cases. A total of 125 cases (88.7%) were diagnosed as presenting with late-stage seizures, occurring from 10 days to three years after TBI (93/141 (66.0%) presented within six months after the TBI, 14/141 (9.9%) between six and twelve months, 22/141 (15.7%) between one and two years and only 12/141 (8.5%) between two and three years after the TBI. The severity of PTE was rated mild, medium, and severe in 3.6%, 6.9%, and 17% of the TBI patients. Multiple regression analysis was carried out to identify factors contributing to the risk of developing PTE. Five parameters contributed to the model: Older age, greater severity of brain injury, abnormal neuroimaging, surgical treatment, and early-stage seizures.ConclusionAge, severity of brain injury, neuroimaging results, treatment methods, and early-stage seizures are independent risk factors of PTE.     

An investigation of the impact of facial affect recognition impairments in moderate to severe TBI on fatigue,depression, and quality of life

Individuals with moderate to severe traumatic brain injury (TBI) have been shown to experience significant problems in facial affect recognition (FAR). However, it is not known how these impairments relate to overall functioning and quality of life (QoL) following TBI. The aim of the current study was to test the hypothesis that worse performance on an FAR task would be associated with reduced QoL (related to social and emotional functioning), worse mood, and increased fatigue. Forty-seven individuals with TBI and 27 healthy controls (HCs) completed the facial emotion identification task (FEIT), as well as questionnaires assessing social and emotional QoL, mood, and fatigue. The TBI group performed significantly worse than HCs on the FEIT. A significant relationship between FAR and fatigue and QoL related to social and emotional functioning was documented, but in an unexpected direction: individuals who performed better on the FEIT reported poorer QoL and greater fatigue. Individuals who have better FAR may require increased effort to perform this task, and thus experience greater fatigue and poorer social and emotional QoL.     

人参总皂苷对大鼠脑外伤后神经细胞凋亡的影响

目的 研究人参总皂苷对脑外伤大鼠神经细胞凋亡的影响,探讨其抑制创伤性脑损伤(TBI)后继发性损伤的作用机制.方法 采用改良的Feeney自由落体法建立脑外伤模型,将Sprague-Dawley大鼠54只按照随机数字表法分为假手术组、脑外伤组、人参总皂苷治疗组(治疗组),每组18只.模型建立后24h处死大鼠,采用干湿重法测量脑水含量,光镜下观察尼氏染色海马细胞形态,凋亡细胞原位末端标记法(TUNEL)和免疫组织化学方法观察大脑皮质、海马神经细胞凋亡及凋亡基因bax、bcl-2、caspase-3的蛋白表达情况.结果 与脑外伤组比较,人参总皂苷治疗后的治疗组脑含水量明显减低,损伤侧海马病理学改变明显减轻,神经细胞凋亡减少,bcl-2的表达增高,bax、caspase-3的表达减少,差异均有统计学意义(P＜0.05).结论 人参总皂苷可以减轻脑外伤后继发性损伤,其机制可能是升高bcl-2的表达,抑制bax、caspase-3的表达,从而阻滞TBI后神经细胞凋亡.     

Clusterin expression is upregulated following acute head injury and localizes to astrocytes in old head injury

There is mounting evidence linking traumatic brain injury (TBI) to neurodegeneration. Clusterin (apolipoprotein J or ApoJ) is a complement inhibitor that appears to have a neuroprotective effect in response to tissue damage and has been reported to be upregulated in Alzheimer's disease. Here we investigated the time course and cellular expression pattern of clusterin in human TBI. Tissue from 32 patients with TBI of varying survival times (from under 30 min to 10 months) was examined using immunohistochemistry for clusterin alongside other markers of neurodegeneration and neuroinflammation. TBI cases were compared to ischemic brain damage, Alzheimer's disease and controls. Double immunofluorescence was carried out in order to examine cellular expression. Clusterin was initially expressed in an axonal location less than 30 min following TBI and increased in intensity and the frequency of deposits with increasing survival time up to 24 h, after which it appeared to reduce in intensity but was still evident several weeks after injury. Clusterin was first evident in astrocytes after 45 min, being increasingly seen up to 48 h but remaining intense in TBI cases with long survival times. Our results suggest clusterin plays a role in modulating the inflammatory response of acute and chronic TBI and that it is a useful marker for TBI, particularly in cases with short survival times. Its prominent accumulation in astrocytes, alongside a mounting inflammatory response and activation of microglial cells supports a potential role in the neurodegenerative changes that occur as a result of TBI.     

Genetic antecedents of dopamine dysfunction in schizophrenia.

BACKGROUND: Relatives of schizophrenic probands frequently manifest attenuated features of this illness including the negative symptoms and the milder positive psychotic symptoms. These two symptom dimensions are hypothesized to be associated with decreased and increased brain dopamine (DA) functions, respectively, raising the possibility that DA abnormalities may be present in the relatives of schizophrenic probands. METHODS: Plasma homovanillic acid (HVA), the major DA metabolite and an indicator of brain DA activity, was measured in nonpsychotic, physically healthy first-degree relatives (n = 55) of schizophrenic probands and in normal subjects (n = 20) without a family history of schizophrenia. RESULTS: Plasma HVA inversely correlated with negative symptoms and positively correlated with attenuated positive symptoms. Also, relatives had decreased plasma HVA compared to normal subjects, consistent with the fact that these relatives are characterized by negative symptoms. These findings were not related to major peripheral factors that could affect plasma HVA suggesting that the findings may reflect changes in brain DA activity. CONCLUSIONS: Negative symptoms indicating a genetic diathesis to schizophrenia in relatives may have a biologic basis in reduced DA activity and the DA dysfunction of schizophrenia may have genetic antecedents. This opens an important new avenue for further study of DA in this illness.     

Longitudinal aspects of emotion recognition in patients with traumatic brain injury

Changes in emotional and social behaviour are relatively common following traumatic brain injury (TBI). Impairments in recognising the emotional state of others may underlie some of the problems in social relationships that these patients experience. The few previous studies examining emotion recognition in TBI typically assessed patients once, long after the onset of brain injury, making it difficult to distinguish the direct effect of brain injury from the effects of environmental changes. This study examined 30 patients with TBI shortly after brain injury and 32 orthopaedic control patients on their recognition of emotions expressed in the face and the voice using discrimination and labelling tasks. These patients were followed up 1 year later to examine the longitudinal development of emotion recognition deficits. TBI patients were found to be impaired on emotion recognition compared to the control patients both early after injury and 1 year later. The fact that impairments in emotion recognition were evident early after TBI and no evidence of recovery over time was found, suggests a direct effect of brain injury.