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Results for “Traumatic Brain Injuries”

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PubMed2000

Impaired auditory gating and P50 nonsuppression following traumatic brain injury.

Traumatic brain injury (TBI) can produce persistent attention and memory impairment that may in part be produced by impaired auditory sensory gating. The P50 evoked waveform response to paired auditory stimuli appears to be a useful measure of auditory gating. The first controlled measurement of the P50 ratio in TBI patients is described: when 20 patients with persistently symptomatic TBI were compared with 20 control subjects, the P50 ratio was significantly greater in the TBI group. The potential neurophysiologic and therapeutic implications of this finding in TBI patients who report symptoms consistent with impaired auditory gating are discussed.

Adult↗

PubMed2001

Reduced hippocampal volume in association with p50 nonsuppression following traumatic brain injury.

Traumatic brain injury (TBI) may produce persistently impaired auditory gating. This cholinergic-dependent, hippocampally mediated preattentive cognitive function that facilitates filtering of auditory stimuli may be indexed by the P50 evoked waveform to paired auditory stimuli. Abnormal P50 suppression post TBI is believed to result from injury to the hippocampus and/or its afferent cholinergic projections. This hypothesis was tested by comparing hippocampal and total brain volumes on MRI between ten P50-nonsuppressing TBI patients and ten normal control subjects matched for age, gender, and education. TBI subjects had highly significant bilateral hippocampal volume reductions, even when covaried for reductions in total brain volume. Degree of volume loss was not correlated with initial TBI severity. Findings support the hypothesis that hippocampal injury underlies P50 nonsuppression post TBI and suggest that such structural abnormalities may be observed even in "mildly" injured persons.

Adult↗

PubMed2005

Cognitive impairment associated with major depression following mild and moderate traumatic brain injury.

Traumatic brain injury (TBI) and major depression are neuropsychiatric conditions that have been associated with cognitive dysfunction. The aim of this study was to explore the relationship between major depression and cognitive impairment following mild and moderate TBI. Seventy-four TBI patients were assessed for the presence of major depression using the Structured Clinical Interview for the DSM-IV and completed a neurocognitive assessment battery. Subjects with major depression (28.4%), compared to those without, were found to have significantly lower scores on measures of working memory, processing speed, verbal memory and executive function. Potential mechanisms and implications for treatment are discussed.

Adolescent↗

PubMed2006

Influence of Angiotensin-converting enzyme polymorphism on neuropsychological subacute performance in moderate and severe traumatic brain injury.

Traumatic brain injury (TBI) frequently results in cerebrovascular lesions that may increase secondary damage and cause neuropsychological impairment. Previous studies suggest an association among the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE), cardiovascular disease, and cognitive performance. Clinical and experimental studies have demonstrated the beneficial effects of ACE inhibitor treatment on vascular injury, hypertension, brain ischemia, and cognitive functioning. In a sample of 73 moderate and severe TBI patients, the authors assessed whether cognitive sequelae differed in relation to the ACE I/D polymorphism. D allele carrier patients performed worse than those with I/I polymorphism on tests involving attention and processing speed. Findings suggest that the physiopathological changes associated with TBI may have greater consequences in ACE D allele carriers.

Adolescent↗

PubMed2004

Is there a sex difference in the course following traumatic brain injury?

Traumatic brain injury (TBI) is a significant cause of death and disability in the United States. Sex has not been thoroughly examined as a factor that may influence outcome following TBI. Clinical studies involving humans that have focused on sex and TBI outcome have yielded inconclusive results, yet sex-related physiologic differences have been demonstrated in animal studies. The purpose of this study is to examine the interaction of sex and age in relation to outcome at 3 and 6 months postinjury in a population of individuals with TBI. The sample includes 157 subjects (124 males, 33 females), 16 to 89 years of age, admitted to a level 1 trauma center following TBI. Physiologic data and information about injury severity and clinical course were gathered during hospitalization. Outcome was assessed at 3 and 6 months postinjury using the Extended Glasgow Outcome Scale (GOSE) and Functional Status Examination (FSE). In this sample, there was a significant relationship between sex and age with respect to functional outcome at 6 months following TBI, controlling for initial injury severity. Females age 30 years or older had significantly poorer outcome as measured by the GOSE (P = 0.031) and the FSE (P = 0.037) than either males or younger females. There was also a very different rate of recovery, with women age 30 years and older, on average, showing no improvement between 3 and 6 months postinjury. Further study is needed to elucidate the reasons why sex may affect outcome following TBI.

Adolescent↗

PubMedDate not supplied

Endothelial cell activation following moderate traumatic brain injury.

Traumatic brain injury (TBI) initiates a cascade of acute and chronic injury responses which include disturbances in the cerebrovasculature that may result in the activation of the microvascular endothelial development of a dysfunction endothelium. The present study examines endothelial cell (EC) activation in a percussion model of moderate TBI. The criteria for endothelial activation used in these studies was surface expression of a number of markers collectively termed endothelial activation antigens. Temporal induction of the major histocompatibility (MHC) class II molecules, E-selectin (CD62E), vascular cell adhesion molecule (VACM-1) (CD106) as well as altered expression of constitutively expressed intercellular adhesion molecule-1 (ICAM-1) (CD54), the glucose transporter protein (glut-1), the transferrin receptor (tfR) (CD71), and MHC class I molecules was examined at various times following impact. Induction of E-selectin and increased expression of ICAM-1 was seen by 2 h post-impact (PI) and was sustained through 24 h PI. Decreased expression of immunologically reactive glut-1 and tfR was observed by 2-4 h PI and remained low up to 24 h PI. No induction of VCAM-1, MHC class II molecules or altered constitutive expression or MHC class I molecules was seen. Changes in EC activation were observed predominantly at the site of impact and were diminished temporarily. These results indicate that mild concussive injury to the brain results in activation of the endothelium.

ATP-Binding Cassette Transporters↗

PubMed2003

Protein accumulation in traumatic brain injury.

Traumatic brain injury (TBI) is one of the most devastating diseases in our society, accounting for a high percentage of mortality and disability. A major consequence of TBI is the rapid and long-term accumulation of proteins. This process largely reflects the interruption of axonal transport as a result of extensive axonal injury. Although many proteins are found accumulating after TBI, three have received particular attention; beta-amyloid precursor protein and its proteolytic products, amyloid-beta (Abeta) peptides, neurofilament proteins, and synuclein proteins. Massive coaccumulations of all of these proteins are found in damaged axons throughout the white matter after TBI. Additionally, these proteins form aggregates in other neuronal compartments and in brain parenchyma after brain trauma. Interestingly, TBI is also an epigenetic risk factor for developing neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease. Here, the similarities and differences of these accumulations with pathologies of neurodegenerative diseases will be explored. In addition, the potential deleterious roles of protein accumulations on functional outcome and progressive neurodegeneration following TBI will be examined.

Amyloid beta-Peptides↗

PubMed2002

Molecular mechanisms in the pathogenesis of traumatic brain injury.

Traumatic brain injury (TBI) is a serious neurodisorder commonly caused by car accidents, sports related events or violence. Preventive measures are highly recommended to reduce the risk and number of TBI cases. The primary injury to the brain initiates a secondary injury process that spreads via multiple molecular mechanisms in the pathogenesis of TBI. The events leading to both neurodegeneration and functional recovery after TBI are generalized into four categories: (i) primary injury that disrupts brain tissues; (ii) secondary injury that causes pathophysiology in the brain; (iii) inflammatory response that adds to neurodegeneration; and (iv) repair-regeneration that may contribute to neuronal repair and regeneration to some extent following TBI. Destructive multiple mediators of the secondary injury process ultimately dominate over a few intrinsic protective measures, leading to activation of cysteine proteases such as calpain and caspase-3 that cleave key cellular substrates and cause cell death. Experimental studies in rodent models of TBI suggest that treatment with calpain inhibitors (e.g., AK295, SJA6017) and neurotrophic factors (e.g., NGF, BDNF) can prevent neuronal death and dysfunction in TBI. Currently, there is still no precise therapeutic strategy for the prevention of pathogenesis and neurodegeneration following TBI in humans. The search continues to explore new therapeutic targets and development of promising drugs for the treatment of TBI.

Brain Injuries↗

PubMed2004

Recent advances in the development of multifactorial therapies for the treatment of traumatic brain injury.

Traumatic brain injury (TBI) is one of the leading causes of death and disability in the industrialised world and remains a major health problem with serious socioeconomic consequences. So far, despite encouraging preclinical results, almost all neuroprotection trials have failed to show any significant efficacy in the treatment of clinical TBI. This may be due, in part, to the fact that most of the therapies investigated have targeted an individual injury factor. It is now recognised that TBI is a very heterogeneous type of injury that varies widely in its aetiology, clinical presentation, severity and pathophysiology. The pathophysiological sequelae of TBI are mediated by an interaction of acute and delayed molecular, biochemical and physiological events that are both complex and multifaceted. Accordingly, a successful TBI treatment may have to simultaneously attenuate many injury factors. Recent efforts in experimental TBI have, therefore, focused on the development of neuropharmacotherapies that target multiple injury factors and thus improve the likelihood of a successful outcome. This review will focus on three such novel compounds that are currently being assessed in clinical trials; progesterone, dexanabinol and dexamethasone, and provide an update on the progress of both magnesium and cyclosporin A.

Animals↗

PubMed2005

Proteomic identification of biomarkers of traumatic brain injury.

Traumatic brain injury (TBI) is a major national health problem without a US Food and Drug Administration-approved therapy. This review summarizes the importance of discovering relevant TBI protein biomarkers and presents logical rationale that neuroproteomic technologies are uniquely suited for the discovery of otherwise unnoticed TBI biomarkers. It highlights that one must make careful decisions when choosing which paradigm (human vs. animal models) and which biologic samples to use for such proteomic studies. It further outlines some of the desirable attributes of an ideal TBI biomarker and discusses how biomarkers discovered proteomically are complementary to those identified by traditional approaches. Lastly, the most important sequela of any proteomically identified TBI biomarker is validation in preclinical or clinical samples.

Animals↗

PubMedDate not supplied

Event-related potential in facial affect recognition: potential clinical utility in patients with traumatic brain injury.

Traumatic brain injury (TBI) frequently leads to deficits in social behavior. Prior research suggests that such deficits may result from impaired perception of basic social cues. However, these social-emotional deficits have not been studied electrophysiologically. We measured the P300 event-related potential (ERP), which has been shown to be a sensitive index of cognitive efficiency, in 13 patients with a history of moderate to severe TBI and in 13 healthy controls. The P300 response was measured during detection of 30 pictures of angry faces (rare target) randomly distributed among 120 neutral faces (frequent nontarget). Compared to control subjects, the TBI group's P300 responses were significantly delayed in latency (p = 0.002) and lower in amplitude (p = 0.003). TBI patients also showed slower reaction times and reduced accuracy when manually signaling their detection of angry faces. Coefficients of variation (CV) for the facial P300 response compared favorably to those of many standard clinical assays, suggesting potential clinical utility. For this study, we demonstrated the feasibility of studying TBI patients' P300 responses during the recognition of facial affect. Compared to controls, TBI patients showed significantly impaired electrophysiological and behavioral responses while attempting to detect affective facial cues. Additional studies are required for clinicians to determine whether this measure is related to patients' psychosocial function in the community.

Affect↗

PubMed2006

Symptom experience and emotional distress after traumatic brain injury.

Traumatic brain injury (TBI) is unexpected and affects nearly 1.5 million Americans annually. Many with seemingly minor injuries incur long-lasting symptoms without clear explanation. This study examined the symptom experience and emotional response of persons with mild-to-moderate TBI and was guided by the University of California San Francisco (UCSF) symptom management model. Using a cross-sectional design with persons recruited from outpatient rehabilitation settings, we found a positive and significant relationship between postinjury symptom frequency and tension/anxiety, anger/hostility and perceived chronic stress, implying a need to understand these relationships over time in order to implement symptom management strategies.

Adolescent↗

PubMed2006

Evaluation of pharmacological treatment strategies in traumatic brain injury.

Traumatic brain injury (TBI) is a devastating disease, predominately affecting young people. Although the prognosis for TBI victims has improved in recent years, many survivors of TBI suffer from emotional, cognitive and motor disturbances and a decreased quality of life. In recent years, there has been a rapid increase in the number of pharmacological targets evaluated in clinically-relevant experimental TBI models, showing improved cognitive and motor outcome and decreased loss of brain tissue. Despite the completion of several recent clinical trials using compounds showing neuroprotection in preclinical studies, pharmaceutical treatment strategies with proven clinical benefit are still lacking. This paper reviews the preclinical pharmacological treatment studies evaluated to date in experimental models of TBI. Although human TBI is a complex and multifaceted disease, these studies provide encouraging translational data suggesting that pharmacological compounds, delivered in a clinically-relevant time window, may improve the outcome of TBI patients.

Animals↗

PubMed2003

4: Rehabilitation after traumatic brain injury.

Traumatic brain injury (TBI) commonly affects younger people and causes life-long impairments in physical, cognitive, behavioural and social function. The cognitive, behavioural and personality deficits are usually more disabling than the residual physical deficits. Recovery from TBI can continue for at least 5 years after injury. Rehabilitation is effective using an interdisciplinary approach, and close liaison with the patient, family and carers. The focus is on issues such as retraining in activities of daily living, pain management, cognitive and behavioural therapies, and pharmacological management. The social burden of TBI is significant, and therefore family education and counselling, and support of patient and carers, is important. General practitioners play an important role in providing ongoing support in the community, monitoring for medical complications, behavioural and personality issues, social reintegration, carer coping skills and return-to-work issues.

Activities of Daily Living↗

PubMed1998

Disorders of Mood After Traumatic Brain Injury.

Traumatic brain injury (TBI) of any severity can result in broad and persisting biopsychosocial sequelae. Post-TBI sequelae impact, to varying degrees, a person's ability to function at home and work, leading to added emotional distress. It is in the context of these biological, interpersonal, and social disruptions that mood disorders can arise. Mood disorders after TBI occur at a greater frequency than in the general population, with estimates approaching 25% to 50% for major depression, 15% to 30% for dysthymia, and 9% for mania. Post-TBI depression and mania appear to embrace a symptom presentation that is similar to non-TBI depression and mania, and the symptoms can be discerned from other neurobehavioral symptoms. TBI-related brain damage consistently involves regions of the brain that are increasingly recognized as important in the regulation of mood, including the frontal cortex, basal ganglia, and temporal lobes. However, there is insufficient information to postulate a specific neuroanatomic model for post-TBI depression and mania. It is the variable nature of TBI-related brain injury, occurring in the context of other relevant factors that limit the ability to make accurate models to predict who will develop a post-TBI mood disorder.

Journal Article↗

PubMed2002

Motor skill and mobility recovery outcomes of children and youth with traumatic brain injury.

Traumatic brain injury (TBI) is a major cause of disability in children. Along with other neurological clinical sequelae, children often exhibit motor skill impairment and limitations in functional mobility following TBI. The purpose of this annotated bibliography is to: (1) familiarize therapists with the literature available regarding motor skill and mobility recovery outcomes for children and adolescents with TBI; (2) assist therapists in the selection of motor skill and mobility outcome assessments for use in clinical practice; and (3) provide therapists with comparisons of outcomes for external benchmarking. A number of reports document motor and mobility recovery outcomes as well as recovery in other domains. Studies vary, however, in design, sample size, number and type of outcome assessments used, time since injury at assessment(s), and the consideration of correlating factors such as age at time of injury and injury severity. Further research is needed to describe clinical, satisfaction and resource utilization outcomes, determine outcome predictors, and provide evidence for therapeutic intervention effectiveness.

Brain Injuries↗

PubMed2002

Agitation, aggression, and disinhibition syndromes after traumatic brain injury.

Traumatic brain injury (TBI) is frequently complicated by disinhibition and aggression. These often profound changes in personality, present obstacles to rehabilitative treatments and community reentry. Syndromal presentations may involve a loss of impulse control, spontaneous aggression, and dysphoric bipolar states. Common neuropathological findings of inferior frontal lobe dysfunction support both disinhibition and kindling models of TBI-induced aggression. Assessment of these highly disruptive symptoms requires detailed historical, clinical, and neuropsychological information to formulate appropriate strategies. Management of TBI-related aggression may involve pharmacological, environmental, and psychotherapeutic strategies that incorporate caregiver training and support.

Aggression↗

PubMed2006

[Hormonal diseases after traumatic brain injury].

Traumatic brain injury represents major medical and social problem in all developed countries. Its incidence is about 200 per 100,000 inhabitants per year. In the acute phase immediately after injury the posterior pituitary dysfunction is well-known. The incidence of severe grossly hypernatremic cases of diabetes insipidus (DI) is about 3%, less severe form of ADH insufficiency was recognized in 21-26%. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) was described in about 14%. These changes are transient in most cases, persisting DI has an incidence of 5-7% and SIADH cases recover almost always. Since the beginning of this century several series evaluating prospectively all patients after moderate to severe TBI have been published. Permanent hypopituitarism was found in one quarter to one half of them. The most common turned out to be the growth hormone (17.6%) and gonadotropic (13.4%) deficiency. Less common is the corticotropic (8.4%) and thyrotropic (4.3%) insufficiency. In the majority of patients an isolated dysfunction was discovered. However, in 9%, a combined failure of two or more HPA axis was present. This paper describes the minimum investigation needed to diagnose hypopituitarism by patients after TBI, who may profit from substitution therapy.

Brain Injuries↗