Recurrent traumatic brain injury

This article reviews, analyses and provides commentary on the most recent literature concerning recurrent traumatic brain injury (RTBI) case histories. It is revealed that a significant proportion of TBI sufferers survive and recover most of the functions of daily living. However, relatively little is known about the epidemiology, effects, or causes of a new phenomenon: recurrent TBI.     

Severe traumatic brain injury

Traumatic brain injury is a leading cause of morbidity and mortality, especially under 45 years of age. The primary brain injury occurs at the moment of trauma and is defined by the direct damage to tissue. In contrast, secondary brain injury develops over time and is accessible to therapeutic interventions. Patients with severe traumatic brain injury have to be transferred to a specialized trauma centre in order to perform appropriate diagnostic and therapeutic procedures. These include surgical management of lesions (e.g. haematoma evacuation) as well as specific neurointensive care. Neurointensive care medicine principles such as treatment of increased intracranial pressure and advanced invasive neuromonitoring of brain tissue have to be followed.     

Work-related deaths and traumatic brain injury

Background: Traumatic brain injury (TBI) at the workplace is a significant contributor to the number of work-related deaths that occur per year. This study aimed to quantify and characterize these deaths in Ontario.

Methods: The study design was a case series with analytic and surveillance components. Data was obtained from the Chief Coroner's Office of Ontario from 1996-2000.

Results: A total of 488 work-related injury fatalities were identified. Evidence of TBI was apparent in 45% of these cases (n = 211). Industries with the highest rate of work-related TBI mortality expressed per 100 000 working population included primary industry (59.1), agriculture (24.5), construction (20.0) and transportation/communications/utilities industries (13.9). Deaths involving TBI were more likely to be due to falls than non-TBI-related deaths among workers (p = 0.0001).

Conclusions: Results from this research indicate that prevention programmes should focus on decreasing falls at all ages and increasing the use of personal protective equipment.     

Corpus striatum and traumatic brain injury

The possibility of a subcortical syndrome differentially affecting memory in traumatic brian injury TBI subjects was examined. Magnetic resonance imaging scans of 46 traumatic brain injured male patients were compared with those of 34 male control subjects. Surface area measurements of the corpus striatum were calculated for both groups. Results demonstrated no significant differences in corpus striatum surface area measurements. Additionally, TBI patients were grouped according to severity of injury, as well as degree of corpus striatum atrophy, and neuropsychological outcome was examined. There were modest (r=0.35) but significant correlations between corpus striatum degeneration and the delayed recall trial and total score of the Rey Auditory Verbal Learning Test, but no other correlations between neuropsychological and corpus striatal surface area were significant. Because subcortical pathology may have a differential effect on memory, recognition and recall memory were further analysed, but no significant differences were found. TBI subjects with the smallest corpus striatum values did not test significantly different from TBI patients with normal corpus striatum values or differences in cortical atrophy, as determined by a ventricle to brain ratio. These findings suggest that there is not a unique pattern of subcortical pathology involving the corpus striatum in TBI.     

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.     

Pathophysiology of traumatic brain injury

The knowledge of the pathophysiology after traumatic head injuryis necessary for adequate and patient-oriented treatment. Asthe primary insult, which represents the direct mechanical damage,cannot be therapeutically influenced, target of the treatmentis the limitation of the secondary damage (delayed non-mechanicaldamage). It is influenced by changes in cerebral blood flow(hypo- and hyperperfusion), impairment of cerebrovascular autoregulation,cerebral metabolic dysfunction and inadequate cerebral oxygenation.Furthermore, excitotoxic cell damage and inflammation may leadto apoptotic and necrotic cell death. Understanding the multidimensionalcascade of secondary brain injury offers differentiated therapeuticoptions.     

Hypertension in traumatic brain injury

The incidence and natural history of hypertension associated with traumatic brain injury were studied using a cohort of 80 patients discharged from a brain-injury rehabilitation centre. Although a significant incidence (15%) of hypertension is documented in traumatic brain-injured patients, the problem appears transient for most patients. Nonetheless, hypertension after brain injury merits treatment while it is an ongoing process for the anticipated few patients in whom it might persist.     

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.     

Neuropsychologists diagnose traumatic brain injury

The case of John versus Im (2002) stands for the proposition that clinical neuropsychologists are not qualified to diagnose traumatic brain injury. This ruling by the Supreme Court of Virginia prohibits neuropsychologists from testifying about these professional conclusions in the courtroom. However, in clinical practice neuropsychologists are often asked to disentangle the relative contribution of brain dysfunction and psychological factors to presenting symptomology. In the proposed submission, the authors provide an analysis of the neuropsychological testimony at issue in John versus Im using the admissibility standards for expert testimony that were established and refined by a trilogy of cases from the Supreme Court of the United States. The paper provides support for the notion that neuropsychological method has an established scientific base of knowledge, standards for clinical competence, and evidence of peer-reviewed acceptance by medical related disciplines. No other scientific discipline has employed a more rigorous methodology for assessing cognitive function and disentangling the relative contributions of brain dysfunction and psychological factors to presenting symptomology. By limiting the testimony of neuropsychologists as to cause of an individual's cognitive impairment, courts will exclude opinions based on scientific research and specialized knowledge that would assist in the trier of fact.     

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.     

Bromocriptine in traumatic brain injury

The authors report the case of a 63-year-old patient with severe traumatic brain injury (TBI) associated with Parkinson's syndrome, whose performances were dramatically improved by bromocriptine therapy, with an improvement of the scores, not only on tests evaluating motor functions but also on tests evaluating the patient's cognitive functions. However, no improvement was observed with levodopa.