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PubMed2006

Serum biochemical markers for post-concussion syndrome in patients with mild traumatic brain injury.

Mild traumatic brain injury (MTBI) is a major public health problem in the United States. A significant subset of MTBI patients develop persistent and distressing neurological, cognitive, and behavioral symptoms, known as the post-concussion syndrome (PCS). To date, multiple studies have assessed the relationship between brain-related proteins found in the serum at the time of injury, and the development of PCS. We conducted a systematic review of prospective cohort studies that assessed the ability of serum biochemical markers to predict PCS after MTBI. A total of 11 studies assessing three different potential biochemical markers of PCS--S100 proteins, neuron-specific enolase (NSE), and cleaved Tau protein (CTP)--met selection criteria. Of these markers, S100 appeared to be the best researched. We conclude that no biomarker has consistently demonstrated the ability to predict PCS after MTBI. A combination of clinical factors in conjunction with biochemical markers may be necessary to develop a comprehensive decision rule that more accurately predicts PCS after MTBI.

Animals↗

PubMed2002

Useful field of view after traumatic brain injury.

BACKGROUND: Traumatic brain injury (TBI) survivors often have sensory and cognitive impairments that may interfere with driving ability. The Useful Field of View (UFOV) is a measure of visual information processing that is a good predictor of vehicle crash risk in older adults. OBJECTIVE: The objective of this study was to explore the possibility that UFOV is compromised after TBI. DESIGN: UFOV performance of 23 TBI survivors and 18 young adults without neurological impairment were compared. CONCLUSION: TBI survivors had higher UFOV scores than young adults, which indicated a greater functional loss of peripheral vision. The results suggest that the UFOV may be a valuable instrument for assessing driving readiness in TBI survivors.

Accidents, Traffic↗

PubMed1997

Hypertonic/hyperoncotic saline attenuates microcirculatory disturbances after traumatic brain injury.

BACKGROUND: Traumatic brain injury (TBI) induces an acute inflammatory response characterized by early recruitment of inflammatory cells (white blood cells). Rapid resuscitation of TBI with hypertonic saline/dextran (HS/DEX) yields promising results in clinical and experimental studies. The purpose of this paper was to test the hypothesis that HS/DEX exerts its effects in part through a modulation of the acute inflammatory response to TBI. METHODS: Rabbits equipped with chronic cranial windows underwent fluid-percussion injury and were followed up for 6 hours. Intravital fluorescence videomicroscopy technique was used to visualize white blood cell trafficking and to measure pia vessel diameters and venular shear rates. Three groups were studied: sham (group I, n = 5), trauma (group II, n = 7), and trauma and 4 mL/kg 7.2% NaCl/10% dextran 60 IV over 5 minutes at 10 minutes after TBI (group III, n = 7). RESULTS: TBI in groups II and III led to significant increases of intracranial pressure. Arteriolar diameters after trauma increased by 17 +/- 8% at 6 hours in group II. Infusion of HS/DEX completely prevented this secondary diameters increase. At 6 hours, the increase of "sticking" white blood cells in group III was reduced by approximately 90% compared with group II. CONCLUSIONS: Whether the anti-inflammatory effect of HS/DEX plays a role in reducing delayed brain damage (> 6 hours after TBI) or other systemic complications of TBI arises as an important question and should be investigated further.

Acute Disease↗

PubMed2000

The biobehavioral correlates of post-traumatic brain injury depression.

Traumatic brain injury (TBI), typically resulting from vehicle accidents or acts of violence, is a major public health concern. Survivors often face lifelong impairments affecting functional status, cognition, and mood. Depression, the most common mood disorder affecting TBI survivors, most likely is underdiagnosed and presents differently than primary depression or depression after other brain insults. Unfortunately, few studies have been reported that advance theoretical perspectives on post-TBI depression. Currently, there is some evidence that neurochemical and anatomical changes contribute to post-TBI depression. Interpersonal factors, such as sense of belonging and social support, may contribute to the incidence of post-TBI depression. Because of limited theoretical viewpoints, advances have not been made in cost-effective and efficient interventions for this mood disorder, which prolongs rehabilitation and contributes to family suffering.

Brain Chemistry↗

PubMed2005

Prevalence of hypopituitarism and growth hormone deficiency in adults long-term after severe traumatic brain injury.

OBJECTIVE: Traumatic brain injury (TBI) has been associated with hypopituitarism and GH deficiency. However, TBI-mediated hypopituitarism may be more frequent than previously thought. The present work, performed in patients with severe TBI at least 1 year before, had three aims: (i) to evaluate the prevalence of hypopituitarism, (ii) in particular to evaluate the prevalence of GH deficiency, and (iii) to compare three different tests of GH reserve in this cohort. DESIGN AND PATIENTS: From a nonselected group of 249 patients admitted to our Clinical Centre for severe TBI over the last 5 years, 200 of them answered a custom made questionnaire of symptoms of hypopituitarism enclosed in the invitation letter to participate in the study. A total of 170 (99 men and 14 women), accepted to participate in the study (study cohort); 57 had normal questionnaires and were not further studied, 14 discontinued the study, and 99 attended the hospital for dynamic tests of pituitary hormone deficiencies. From these, 44 subjects with IGF-I in the lower range were tested with GHRH+GHRP-6; ITT; and glucagon tests of GH reserve, on three different occasions. MEASUREMENTS: Pituitary hormones plus IGF-I and target gland hormones were analysed. RESULTS: With regard to the initial cohort of 170 subjects (100%), three (1.7%) showed diabetes insipidus; 10 (5.8%) TSH deficiency, 11 (6.4%) ACTH deficiency and 29 (17%) gonadotrophin deficiency. In 10 subjects (5.8%), GH deficiency was diagnosed by strict criteria. Finally, 15 (8.8%) showed combined deficit of several hormones. CONCLUSION: After severe head trauma, gonadotrophin deficiency was the most common pituitary deficit. GH deficiency showed a prevalence similar to ACTH and TSH deficits, i.e. near 6% of the cohort. Taken together, 24.7% of the subjects studied showed any type of pituitary hormone deficiency.

Adult↗

PubMed1998

The management of minor traumatic brain injury.

Minor traumatic brain injury accounts for the majority of the one million head trauma attendances at A&E departments in the United Kingdom. Guidelines have been established listing criteria for skull films, admission to hospital, computed tomography, and neurosurgical consultation. These are currently undergoing revision and were the subject of a satellite symposium to the J Douglas Miller memorial meeting held in October 1996 in Edinburgh. In the East Anglia Region the current guidelines have been issued as memo-cards for A&E officers. The aim of admission is to observe for deterioration, predominantly caused by intracranial haematomas. The indicators for the development of such lesions are an impaired level of consciousness and presence of a skull fracture. Such patients should therefore undergo regular and frequent neurological observations, and be admitted for at least 12 hours. Following discharge, routine follow up should be considered to identify and treat patients with postconcussion symptoms and signs. The possible way forward for the management of these patients is adopting a greater emphasis on preventative aspects, and establishing, implementing, and auditing evidence based guidelines. Improved teaching in the form of formal induction seminars and computerised teaching aids is required, and a better understanding of the aetiology and treatment of the postconcussion syndrome.

Brain Injuries↗

PubMed2003

A review of cholinergic agents in the treatment of neurobehavioral deficits following traumatic brain injury.

Although traumatic brain injury (TBI) frequently results in significant handicap, empirical investigations of pharmacological treatment of the neurobehavioral sequelae of TBI are rare. This review presents evidence that supports hypotheses of a cholinergic mechanism underlying some neurobehavioral sequelae of TBI, as well as a critical review of the preliminary evidence supporting the efficacy of cholinergic agents in TBI. Despite numerous methodological limitations, preliminary evidence exists for the efficacy of cholinergic agents in ameliorating attention and memory deficits following TBI. The authors highlight the need for large, randomized, double-blind, placebo-controlled trials that include a broad range of cognitive and behavioral outcome measures.

Amnesia↗

PubMed2005

Genomic responses in rat cerebral cortex after traumatic brain injury.

BACKGROUND: Traumatic brain injury (TBI) initiates a complex sequence of destructive and neuroprotective cellular responses. The initial mechanical injury is followed by an extended time period of secondary brain damage. Due to the complicated pathological picture a better understanding of the molecular events occurring during this secondary phase of injury is needed. This study was aimed at analysing gene expression patterns following cerebral cortical contusion in rat using high throughput microarray technology with the goal of identifying genes involved in an early and in a more delayed phase of trauma, as genomic responses behind secondary mechanisms likely are time-dependent. RESULTS: Among the upregulated genes 1 day post injury, were transcription factors and genes involved in metabolism, e.g. STAT-3, C/EBP-delta and cytochrome p450. At 4 days post injury we observed increased gene expression of inflammatory factors, proteases and their inhibitors, like cathepsins, alpha-2-macroglobulin and C1q. Notably, genes with biological function clustered to immune response were significantly upregulated 4 days after injury, which was not found following 1 day. Osteopontin and one of its receptors, CD-44, were both upregulated showing a local mRNA- and immunoreactivity pattern in and around the injury site. Fewer genes had decreased expression both 1 and 4 days post injury and included genes implicated in transport, metabolism, signalling, and extra cellular matrix formation, e.g. vitronectin, neuroserpin and angiotensinogen. CONCLUSION: The different patterns of gene expression, with little overlap in genes, 1 and 4 days post injury showed time dependence in genomic responses to trauma. An early induction of factors involved in transcription could lead to the later inflammatory response with strongly upregulated CD-44 and osteopontin expression. An increased knowledge of genes regulating the pathological mechanisms in trauma will help to find future treatment targets. Since trauma is a risk factor for development of neurodegenerative disease, this knowledge may also reduce late negative effects.

Animals↗

PubMed2006

Systematic review of prognostic models in traumatic brain injury.

BACKGROUND: Traumatic brain injury (TBI) is a leading cause of death and disability world-wide. The ability to accurately predict patient outcome after TBI has an important role in clinical practice and research. Prognostic models are statistical models that combine two or more items of patient data to predict clinical outcome. They may improve predictions in TBI patients. Multiple prognostic models for TBI have accumulated for decades but none of them is widely used in clinical practice. The objective of this systematic review is to critically assess existing prognostic models for TBI METHODS: Studies that combine at least two variables to predict any outcome in patients with TBI were searched in PUBMED and EMBASE. Two reviewers independently examined titles, abstracts and assessed whether each met the pre-defined inclusion criteria. RESULTS: A total of 53 reports including 102 models were identified. Almost half (47%) were derived from adult patients. Three quarters of the models included less than 500 patients. Most of the models (93%) were from high income countries populations. Logistic regression was the most common analytical strategy to derived models (47%). In relation to the quality of the derivation models (n:66), only 15% reported less than 10% pf loss to follow-up, 68% did not justify the rationale to include the predictors, 11% conducted an external validation and only 19% of the logistic models presented the results in a clinically user-friendly way CONCLUSION: Prognostic models are frequently published but they are developed from small samples of patients, their methodological quality is poor and they are rarely validated on external populations. Furthermore, they are not clinically practical as they are not presented to physicians in a user-friendly way. Finally because only a few are developed using populations from low and middle income countries, where most of trauma occurs, the generalizability to these setting is limited.

Brain Injuries↗

PubMed1997

Medical management of noncognitive sequelae of minor traumatic brain injury.

Mild traumatic brain injury (TBI) encompasses the postconcussion syndrome characterized by symptoms that include a variety of physical symptoms as well as cognitive and behavioral impairments. The focus of this discussion is on the medical management of posttraumatic headaches, posttraumatic seizures, dizziness, auditory impairments, anosmia, tremor, paraspinal pain, and visual symptoms. Adjustment disorders with disturbances of affect and emotion lability also may accompany mild TBI. All of these conditions may be approached with medications or a variety of therapy techniques or both. The approach to concussion in sports-related injuries is also reviewed.

Journal Article↗

PubMed2002

Mild traumatic brain injury.

Mild traumatic brain injury is frequently seen in an athletic population, especially in contact sports. Many underlying pathophysiologic mechanisms have been identified. Several injury classification schemes have been proposed, yet severity grading and management remain controversial. Although second-impact syndrome is the driving force behind conservative management by many clinicians, athletes suffer more commonly from postconcussive syndrome. Recent research has examined the diagnostic value of several available tests, including electroencephalogram, magnetic resonance imaging, and neuropsychologic testing, with variable results. Neuropsychologic testing has shown promise in evaluating cognitive function when baseline studies are obtained and compared with postinjury examinations. Treatment of postconcussive symptoms with selective serotonin reuptake inhibitors has also been tested, with favorable results.

Athletic Injuries↗

PubMed2004

The role of the helmet in the prevention of traumatic brain injuries.

Today, traumatic brain injuries (TBIs) exceed 1 million cases per year. Tens of thousands of people die and hundreds of thousands of people are hospitalized. The health care costs exceed US dollars 50 billion. The Centers for Disease Control and Prevention estimate that people with mild TBIs who are not hospitalized add another US dollars 17 billion to the total dollars spent on care. These high frequencies and costs place a high priority on programs and procedures to minimize the number of injuries and to reduce the severity of those that occur. One of these programs focuses on the protective devices worn by the people that work and play in environments where there is an identified risk of TBI. Because these environments cover a wide variety of activities, the design and effectiveness of these protective devices must be specific to the nature of the activity and the person they are designed to protect.

Accidents, Occupational↗

PubMed2006

Inhibition of caspase-mediated apoptosis by peroxynitrite in traumatic brain injury.

In traumatic brain injury (TBI), neurons surviving the primary insult may succumb through poorly understood secondary mechanisms. In vitro, cortical neurons exposed to stretch injury exhibited enhanced vulnerability to NMDA, apoptotic-like DNA fragmentation, peroxynitrite (PN) formation, and cytoplasmic cytochrome c accumulation. Surprisingly, caspase-3 activity was undetectable by both immunoblotting and fluorogenic activity assays. Therefore, we hypothesized that PN directly inhibits caspases in these neurons. Consistent with this, stretch injury in cultured neurons elicited tyrosine nitration of procaspase-3, but not caspase-9 or Apaf-1, suggesting a direct interaction of PN with caspase-3. In an ex vivo system, PN inhibited the activity of caspase-3, and this inhibition was reversible with the addition of the sulfhydryl reducing agent dithiothreitol, indicating that PN inhibits caspases by cysteinyl oxidation. Moreover, in cultures, the PN donor 3-morpholinosydnonimine (SIN-1) blocked staurosporine-induced caspase-3 activation and its downstream effects including PARP-1 [poly-(ADP-ribose) polymerase-1] cleavage and phosphotidylserine inversion, suggesting that peroxynitrite can inhibit caspase-3-mediated apoptosis. To examine these mechanisms in vivo, rats were exposed to a lateral fluid percussion injury (FPI). FPI caused increased neuronal protein nitration that colocalized with TUNEL staining, indicating that PN was associated with neurodegeneration. Caspase-3 activity was inhibited in brain lysates harvested after FPI and was restored by adding dithiothreitol. Our data show that caspase-mediated apoptosis is inhibited in neurons subjected to stretch in vitro and to TBI in vivo, mostly because of cysteinyl oxidation of caspase-3 by PN. However, this is insufficient to prevent cell death, indicating that the TBI therapy may, at a minimum, require a combination of both anti-apoptotic and anti-oxidant strategies.

Animals↗

PubMedDate not supplied

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.

Athletic Injuries↗

PubMed2002

Reversal of attenuation of cerebrovascular reactivity to hypercapnia by a nitric oxide donor after controlled cortical impact in a rat model of traumatic brain injury.

OBJECT: Traumatic brain injury (TBI) attenuates the cerebral vasodilation to hypercapnia. Cortical spreading depression (CSD) also transiently reduces hypercapnic vasodilation. The authors sought to determine whether the CSD elicited by a controlled cortical impact (CCI) injury masks the true effect of TBI on hypercapnic vasodilation, and whether a nitric oxide (NO) donor can reverse the attenuation of hypercapnic vasodilation following CCI. METHODS: Anesthetized rats underwent moderate CCI. Cerebral blood flow was monitored with laser Doppler flowmetry and the response to hypercapnia was determined for injured and sham-injured animals. The effect of the NO donor, S-nitroso-N-acetylpenicillamine (SNAP), on this response was also assessed. At an uninjured cortical site ipsilateral to the CCI, a single wave of CSD was recorded and the CO2 response at this location was significantly attenuated for up to 30 minutes (seven rats, p < 0.05). At the injured cortex, hypercapnic vasodilation continued to be attenuated for 7 hours. The cerebral vasodilation to CO2 was 37 +/- 5% in injured rats (six) compared with 84 +/- 10% in the sham-injured group (five rats, p < 0.05). After 30 minutes of topical superfusion with SNAP, hypercapnic vasodilation was restored to 74 +/- 7% (nine rats, p > 0.1 compared with that in the sham-injured group). In contrast, papaverine, an NO-independent vasodilator, failed to reverse the attenuation of the CO2 response to CCI. CONCLUSIONS: The authors conclude that CSD elicited by CCI can mask the true effect of TBI on hypercapnic vasodilation for at least 30 minutes. Exogenous NO, but not papaverine, can reverse the attenuation of cerebrovascular reactivity to CO2 caused by TBI. This result supports the hypothesis that NO production is reduced after TBI and that the NO donor has a potential beneficial role in the clinical management of head injury.

Animals↗

PubMed1999

Physiatric management of mild traumatic brain injury.

Mild traumatic brain injury (MTBI) is a common condition, afflicting as many as 1.5 million Americans yearly. Most individuals sustain MTBI as a result of motor vehicle collisions, but it may also occur as a result of falls, physical assault or sporting accidents. Problems related to MTBI include various pain syndromes, cognitive impairments, disorders of affect, cranial nerve dysfunction, and vertigo, arising from injury to the brain, head, or cervical spine. Symptoms are usually transient, although a small percentage of afflicted individuals develop long-lasting problems, often preventing them from leading productive lives. Recognition of these problems as arising from MTBI is difficult due to the frequent lack of abnormal findings on diagnostic tests and failure to identify a history of head trauma. The American Congress of Rehabilitation Medicine has defined MTBI, an important first step in identifying individuals who need treatment. Diagnosis is usually made by directed questions regarding trauma history and careful procurement and interpretation of appropriate tests. Once a diagnosis is made, proper care can be prescribed in order to lead patients toward more productive lives.

Brain Injuries↗

PubMed1999

Indomethacin: a review of its cerebral blood flow effects and potential use for controlling intracranial pressure in traumatic brain injury patients.

Traumatic brain injury (TBI) causes about 75,000 deaths and leaves approximately 200,000 people disabled in USA each year. Brain swelling and increased intracranial pressure (ICP) contribute to this morbidity and mortality. Aggressive management protocols, including ICP control, have been shown to reduce the overall mortality from 50% to 36% following severe head injury. Despite these encouraging results, new and improved pharmacologic strategies to control ICP are required. Indomethacin (IND) is a non-steroidal anti-inflammatory agent with unique effects on cerebral blood flow physiology which may be of benefit in reducing elevated ICP in TBI patients. Data from animal models and randomized, controlled studies with pre-term infants have shown that i.v. IND produces rapid, significant reductions in cerebral blood flow (CBF). Controlled studies of i.v. IND in normal volunteers show a reduction in CBF from 26%-40%. Case series involving severe TBI patients suggest that IND i.v. boluses of 30-50 mg reduce ICP by 37%-52%, reduce CBF by 22%-26%, with a modest 14% increase in cerebral perfusion pressure (CPP). Despite these encouraging results, i.v. IND should only be considered an experimental treatment for control of refractory ICP in TBI patients. Larger, well-designed randomized trials in TBI patients will provide more efficacy and safety data and delineate the effects of IND alone or in combination with other proven, effective, or experimental therapies. Once these concerns have been addressed, larger outcome studies will ultimately be needed to determine the role of IND for ICP control in TBI patients.

Adult↗

PubMed2000

Validation of the Service Obstacles Scale for the traumatic brain injury population.

Traumatic brain injury is a leading cause of death and disability in the United States. Limited access to specialized medical and rehabilitation services has been linked to poor outcomes. Literature provides little guidance for assessment of service obstacles and satisfaction with community resources. The present investigation describes the development of a specialized scale to evaluate caregivers' perceptions of brain injury services in the community. Results indicate good internal consistency and criterion-related validity of the Service Obstacles Scale. Lack of money for services and lack of adequate community resources were the greatest concerns voiced by respondents, while lack of transportation was the least problematic. Comparisons are made with regard to family needs and respondents' post-injury life quality. Implications for future research are discussed.

Journal Article↗