Progress in brain research
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Among the secondary events occurring after traumatic brain injury (TBI) pathologically increased intracranial pressure (ICP) correlates most closely with poor outcome. In addition to infusion of hypertonic solutions, e.g. mannitol, and other medical measures, decompression of the brain by surgical removal of a portion of the cranium (craniectomy) has been used for many decades as an intuitive strategy for the treatment of post-traumatic ICP increase. The lack of evidence-based clinical and controversial experimental data, however, resulted in decompressive craniectomy to be recommended by most national and international guidelines only as a third tier therapy for the treatment of pathologically elevated ICP. ⋯ The aim of the current review was therefore to summarize and discuss recent experimental data dealing with the use of decompression craniectomy following TBI. The present results suggest that surgical decompression effectively prevents secondary brain damage when performed early enough. Although caution should be taken when transferring conclusions drawn from experimental settings to the clinical situation, the current literature suggests that the timing of decompression may be of utmost importance in order to exploit the full neuroprotective potential of craniectomy following TBI.
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Review
Progressive damage after brain and spinal cord injury: pathomechanisms and treatment strategies.
The pathophysiology of brain and spinal cord injury (SCI) is complex and involves multiple injury mechanisms that are spatially and temporally specific. It is now appreciated that many of these injury mechanisms remain active days to weeks after a primary insult. Long-term survival studies in clinically relevant experimental studies have documented the structural changes that continue at the level of the insult as well as in remote brain structures. ⋯ The progressive changes in multiple structures after brain and SCI are important because of their potential consequences on chronic or developing neurological deficits associated with these insults. In addition, the better understanding of these injury cascades may one day allow new treatments to be developed that can inhibit these responses to injury and hopefully promote recovery. This chapter summarizes some of the recent data regarding progressive damage after CNS trauma and mechanisms underlying these changes.
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Preterm birth is a risk factor for deficits of neurological and cognitive development. Four cohort studies are reported investigating the effects of very premature birth (<32 weeks gestation) on visual, visuocognitive and visuomotor function between birth and 6-7 years of age. The first study used two measures of early visual cortical function, orientation reversal visual event-related potentials (OR-VERP) and fixation shifts under competition. ⋯ Development was generally relatively normal on language tests and on WPPSI scores. Factor analysis showed that while general cognitive ability accounted for the largest part of the variance, significant deficits, and a relationship to MRI results, were primarily in spatial, motor, attention and executive function tests. A model is proposed suggesting that the cluster of deficits seen in children born prematurely may be related to networks involving the cortical dorsal stream and its connections to parietal, frontal and hippocampal areas.
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Traumatic brain injury (TBI) represents one of most common disorders to the central nervous system (CNS). Despite significant efforts, though, an effective clinical treatment for TBI is not yet available. ⋯ In this paper, we review the available in vitro models to study TBI, discuss their biomechanical basis for human TBI, and review the findings from these in vitro models. Finally, we synthesize the current knowledge and point out possible future directions for this group of models, especially in the effort toward developing new therapies for the traumatically brain injured patient.
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Fever is a common occurrence in patients following brain and spinal cord injury (SCI). In intensive care units, large numbers of patients demonstrate febrile periods during the first several days after injury. Over the last several years, experimental studies have reported the detrimental effects of fever in various models of central nervous system (CNS) injury. ⋯ Thus, increased emphasis on the ability to monitor CNS temperature and prevent periods of fever has gained increased attention in the clinical literature. Cooling blankets, body vests, and endovascular catheters have been shown to prevent elevations in body temperature in some patient populations. This chapter will summarize evidence regarding hyperthermia and CNS injury.