Visual imagery as a cognitive means of compensation for brain injury

In this article we are interested in presenting a cognitive therapeutic approach to cases of brain damage based in essence on the principle of compensation, as opposed to the usual cognitive treatment methods which attempt direct treatment of the damaged link in the thinking process. The present case is a patient who suffered a left fronto-temporal injury, resulting in severe problems with understanding verbal material, and who was taught to use the undamaged right hemisphere to translate the verbal material into visual material. He was then instructed to 're-translate' the processed material that he understood back into verbal material. The use of this treatment method is based on the principle of dual coding, which allows for a more meaningful consolidation of learned material. Additionally, it is crucial that the material used within this treatment approach be meaningful to the patient, in order that his motivation be increased.     

Self-regulatory learning and generalization for people with brain injury

Primary objective : Brain injury can result in the loss of previous learnt behaviours that affect an individual's daily functioning. The use of self-regulation helps the individual to relearn the lost behaviours by bringing him/her to self-conscious level through independent and reflective learning derived using a social cognitive perspective. The purpose of this paper is to report on clinical observations made with the use of self-regulation in people with brain injury during the relearning of lost functions.

Methods and procedures : Daily tasks were used to assess the relearning ability of the subjects pre- and post-programme.

Experimental intervention : One-week self-regulatory training on five selected daily tasks.

Main outcomes and results : These provisory observations would suggest that, with specific guidance for people with different needs, such as with impaired cognitive function and depression, self-regulation is effective in enhancing their relearning.

Conclusion : Self-regulatory training is effective in enhancing the relearning of lost functions.     

Comparison of pocket-computer memory aids for people with brain injury

Two styles of pocket computer memory aid were compared as support for people who had sustained non-progressive, closed-head brain injury. A purpose-designed interface provided a diary with auditory alarms, a notebook and links between diary entries and specific notepages. One computer had a physical keyboard, the other did not. Twelve adult volunteers were loaned each computer for 2 months, with a 1 month gap between, in counterbalanced order. It was found that all participants could use the memory aids, and most (83%) found them useful. Little customizing was needed, but amount of use varied widely. Predictors of usage included use of other reminding systems before joining the project, and speed in calculator addition which may reflect working memory. High users preferred the computer with a physical keyboard; low users made more entries with the palm-size computer. These data highlight the need to distinguish ability to use from willingness to use.     

Positive supports for people who experience behavioral and cognitive disability after brain injury: a review

BACKGROUND: Behavioral and cognitive problems are among the most common and troubling consequences of traumatic brain injury. Furthermore, behavioral and cognitive challenges typically interact in complex ways, necessitating an integrated approach to intervention and support. OBJECTIVES: This article reviews literature on behavioral outcome in children and adults with traumatic brain injury, traditional approaches to behavioral intervention and cognitive rehabilitation, and the history, principles, and assessment and treatment procedures associated with context-sensitive, support-oriented approaches to behavioral and cognitive intervention. We propose a clinical framework that integrates cognitive and behavioral intervention themes.     

Imaging after brain injury

Head injury remains an important cause of death and disabilityin young adults. This review will discuss the role of structuralimaging using computed tomography (CT) and magnetic resonanceimaging (MRI) and physiological imaging using CT perfusion,¹³¹Xe CT, MRI and spectroscopy (MRS), single photon emissioncomputed tomography, and positron emission tomography (PET)in the assessment, management, and prediction of outcome afterhead injury. CT allows rapid assessment of brain pathology whichensures patients who require urgent surgical intervention receiveappropriate care. Although MRI provides greater spatial resolution,particularly within the posterior fossa and deep white matter,a complete assessment of the burden of injury requires imagingof cerebral physiology. Physiological imaging techniques canonly provide ‘snap shots’ of physiology within theinjured brain, but they can be repeated, and such data can beused to assess the impact of therapeutic interventions. Perfusionimaging based on CT techniques (xenon CT and CT perfusion) canbe implemented easily in most hospital centres, and providequantitative perfusion data in addition to structural images.PET imaging provides unparalleled insights into cerebral physiologyand pathophysiology, but is not widely available and is primarilya research tool. MR technology continues to develop and is becominggenerally available. Using a complex variety of sequences, MRcan provide data concerning both structural and physiologicalderangements. Future developments with such imaging techniquesshould improve understanding of the pathophysiology of braininjury and provide data that should improve management and predictionof functional outcome.     

颅脑外伤后进展性脑损害的研究进展

颅脑外伤后进展性脑损害,包括脑出血、脑缺血、脑水肿,都是影响颅脑外伤预后的重要因素.本文复习文献,对颅脑外伤后进展性脑损害的发病率、发生机制、早期诊断方法、治疗和预后等相关问题的研究进展进行了综述.     

Neurogenesis after traumatic brain injury

With the hope of replacing neurons lost in traumatic brain injury (TBI), experimental models are being used to investigate TBI-induced neurogenesis. Although selectively vulnerable to TBI, the neurogenic hippocampus may have the unique ability to replace damaged neurons locally. Injury may also activate signaling pathways that induce neuroblasts from the subventricular zone to migrate to areas of focal cortical damage. Additionally, there is some evidence for local activation of latent neural progenitor cells in the injured neocortex itself. Each of these themes is discussed, with emphasis on the possibility of future therapeutic intervention.     

Apoptosis after traumatic brain injury

Apoptosis of neurons and glia contribute to the overall pathology of traumatic brain injury (TBI) in both humans and animals. In both head-injured humans and following experimental brain injury, apoptotic cells have been observed alongside degenerating cells exhibiting classic necrotic morphology. Neurons undergoing apoptosis have been identified within contusions in the acute port-traumatic period, and in regions remote from the site of impact in the days and weeks after trauma. Apoptotic oligodendrocytes and astrocytes have been observed within injured white matter tracts. We review the regional and temporal patterns of apoptosis following TBI and the possible mechanisms underlying trauma-induced apoptosis. While excitatory amino acids, increases in intracellular calcium, and free radicals can all cause cells to undergo apoptosis, in vitro studies have determined that neural cells can undergo apoptosis via many other pathways. It is generally accepted that a shift in the balance between pro- and anti-apoptotic protein factors towards the expression of proteins that promote death may be one mechanism underlying apoptotic cell death. The effect of TBI on regional cellular patterns of expression of survival promoting-proteins such as Bcl-2, Bcl-xL, and extracellular signal regulated kinases, and death-inducing proteins such as Bax, c-Jun N-terminal kinase, tumor-suppressor gene, p53, and the caspase family of proteases are reviewed. Finally, in light of pharmacologic strategies that have been devised to reduce the extent of apoptotic cell death in animal models of TBI, our review also considers whether apoptosis may serve a protective role in the injured brain.     

Chlorpromazine-induced psychosis after brain injury

Antipsychotic agents, most often used for treatment of schizophrenia, are sometimes prescribed for the agitated patient with an organic brain disorder. We report the case of a brain-injured patient who was prescribed chlorpromazine for agitation and who developed a delusional state while taking this antipsychotic agent. The emergence of this delusional state coincided with the exacerbation of certain cognitive deficits. Possible mechanisms for this phenomenon are discussed. Caution is advised when prescribing neuroleptics for patients with traumatic brain injury, especially those agents with significant cognitive side-effects or with a significant potential to precipitate seizures.     

Coagulopathy after traumatic brain injury

Traumatic brain injury has long been associated with abnormal coagulation parameters, but the exact mechanisms underlying this phenomenon are poorly understood. Coagulopathy after traumatic brain injury includes hypercoagulable and hypocoagulable states that can lead to secondary injury by either the induction of microthrombosis or the progression of hemorrhagic brain lesions. Multiple hypotheses have been proposed to explain this phenomenon, including the release of tissue factor, disseminated intravascular coagulation, hyperfibrinolysis, hypoperfusion with protein C activation, and platelet dysfunction. The diagnosis and management of these complex patients are difficult given the lack of understanding of the underlying mechanisms. The goal of this review is to summarize the current knowledge regarding the mechanisms of coagulopathy after blunt traumatic brain injury. The current and emerging diagnostic tools, radiological findings, treatment options, and prognosis are discussed.     

Validation of the stroke drivers screening assessment for people with traumatic brain injury

Cognitive impairments resulting from brain injury affect driving performance. The question of fitness to drive often arises during rehabilitation. Healthcare professionals need reliable criteria against which decisions about driving fitness can be made. Nouri et al. developed the Stroke Drivers Screening Assessment (SDSA), which was found predictive of on-road driving performance in stroke patients. The purpose of this study was to determine whether the SDSA, either alone or combined with other tests, predicted fitness to drive in brain injured people. Fifty-two participants were assessed on the SDSA plus additional cognitive tests. Their fitness to drive was examined on the public road. The SDSA predictions based on equations developed for stroke patients were not an accurate predictor of road test performance. Discriminant analysis was used to identify tests predictive of fitness to drive. Results indicated that a combination of the SDSA, the Stroop and the AMIPB Information Processing tasks correctly classified 87% of cases and may be useful predictors of driving fitness following brain injury. However, cross-validation on an independent sample of people with brain injury is required.     

创伤性脑损伤后肺损伤的发病机制研究进展

背景 创伤性脑损伤(traumatic brain injury,TBI)患者可能发生肺损伤,严重时甚至发生肺功能障碍.脑与肺通过复杂途径相互联系.发生肺功能障碍的TBI患者病死率增加、 加强治疗病房住院时间延长且神经预后较差.目的 综述TBI后肺损伤的研究进展.内容 讨论TBI后肺损伤的发生特点并综述其潜在机制.趋向 根据具体情况评估TBI患者发生肺损伤的潜在风险,并在其临床症状出现前进行相应干预有助于降低发生TBI后肺损伤的风险.     

The brain hypothermia therapy for prevention of vegetation after severe brain injury]

We have presented a new concept of brain hypoxia oriented brain hypothermia treatments. All severe brain injury patients (148 cases) were GCS < 6. The masking brain hypoxia by brain thermo pooling, catecholamine surge induced cardiac dysfunction and intestinal vasodilatation, reduction of Hb-2.3 diphosphoglyserate were major target of initial treatment. These specific brain hypoxia was only controlled by brain hypothermia (34-32 degrees C), oxygen delivery > 800 ml/min. and AT-III > 100%. 2. The brain hypothermia were very successful to prevent masking brain hypoxia, selective radical attack to A10 dopamine nervous system, and brain edema. However, metabolic shift to lipid metabolism and lower growth hormone related immune crisis were recorded as a negative factors. Clinical results were so advanced. The mortality were 44 in 148 cases (30%), good recovery were 59 in 148 cases (40%), mild disability were 20 in 148 cases (13%) and vegetate state were only 15 in 148 cases (10%). The combination of brain hypothermia and replacement of cerebral dopamine were very successful to prevent the vegetation in severe brain injury.     

Lipid peroxidation early after brain injury

The role of lipid peroxidation after brain injury is still not completely understood, and results of different studies have been equivocal. In this study, three proposed peroxidation markers were determined in patients early after isolated head injury and results compared to healthy controls. Malondialdehyde (MDA) and thiobarbituric acid-reactive substances (TBARS) were measured in plasma, and n-pentane was determined in patients' exhaled air. For MDA and TBARS no significant differences could be shown (0.267 vs. 0.358 ng/mL, and 0.896 vs. 0.814 ng/mL in patients vs. healthy volunteers, respectively). n-Pentane, however, was significantly increased in the expired air of patients (0.471 vs. 0.118 nmol/L in healthy volunteers). Similar results for n-pentane were obtained when only male patients and volunteers were considered (0.510 vs. 0.113 nmol/L). Stratification according to clinical outcome showed significantly higher values for n-pentane in male patients with poor outcome (0.656 nmol/L) in comparison with healthy male volunteers (0.113 nmol/L). No difference was found when patients were stratified according to the presence or absence of subarachnoid hemorrhage. It is concluded that, only in a sub-population of patients with brain injury, lipid-peroxidation is a crucial mechanism. n-Pentane seems to be a valuable marker to detect lipid peroxidation early after brain trauma. Malondialdehyde may be of value only later in the course of the disease. TBARS are not a specific marker and should therefore not be used.