Progress in brain research
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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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Deliberate hyperthermia has been used clinically as experimental therapy for neoplastic and infectious diseases. Several case fatalities have occurred with this form of treatment, but most were attributable to systemic complications rather than central nervous system toxicity. Nonetheless, demyelating peripheral neuropathy and neurological symptoms of nausea, delirium, apathy, stupor, and coma have been reported. ⋯ Furthermore, in the neurosurgical intensive-care unit fever is extremely common whereas antipyretic therapy is only poorly effective. Therefore maintaining strict normothermia may be an impossible goal in many patients. Although there are several physiological arguments for avoiding exogenous hyperthermia in neurologically injured patients, there is no evidence that aggressive attempts at controlling spontaneous fever can improve clinical outcome.
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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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Traumatic brain injury (TBI) and traumatic spinal cord injury (SCI) are acquired when an external physical insult causes damage to the central nervous system (CNS). Functional disabilities resulting from CNS trauma are dependent upon the mode, severity, and anatomical location of the mechanical impact as well as the mechanical properties of the tissue. Although the biomechanical insult is the initiating factor in the pathophysiology of CNS trauma, the anatomical loading distribution and the resulting cellular responses are currently not well understood. ⋯ Correlation of insult parameters with cellular changes and subsequent deficits may lead to refined tolerance criteria and facilitate the development of improved protective gear. In addition, advancements in the understanding of injury biomechanics are essential for the development and interpretation of experimental studies at both the in vitro and in vivo levels and may lead to the development of new treatment approaches by determining injury mechanisms across the temporal spectrum of the injury response. Here we discuss basic concepts relevant to the biomechanics of CNS trauma, injury models used to experimentally simulate TBI and SCI, and novel multilevel approaches for improving the current understanding of primary damage mechanisms.
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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.