Progress in brain research
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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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Minor traumatic brain injury (mTBI) is caused by inertial effects, which induce sudden rotation and acceleration forces to and within the brain. At less severe levels of injury, for example in mTBI, there is probably only transient disturbance of ionic homeostasis with short-term, temporary disturbance of brain function. With increased levels of severity, however, studies in animal models of TBI and in humans have demonstrated focal intra-axonal alterations within the subaxolemmal, neurofilament and microtubular cytoskeletal network together with impairment of axoplasmic transport. ⋯ In ice hockey, current return-to-play guidelines do not take into account these new findings appropriately, for example allow returning to play in the same game. It has recently been hypothesized that the processes summarized above may predispose brain cells to assume a vulnerable state for an unknown period after mild injury (mTBI). Therefore, we recommend that any confused player with or without amnesia should be taken off the ice and not be permitted to play again for at least 72h.
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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.
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Before energy metabolism can take place, brain cells must be supplied with oxygen and glucose. Only then, in combination with normal mitochondrial function, sufficient energy (adenosine tri-phosphate (ATP)) can be produced. Glucose is virtually the sole fuel for the human brain. ⋯ This review focuses on three main issues: (1) Cerebral oxygen transport (CBF, and oxygen partial pressure (PO2) and delivery to the brain); (2) Energy metabolism (glycolysis, mitochondrial function: citric acid cycle and oxidative phosphorylation); and (3) The role of the above in the pathophysiology of severe head injury. Basic understanding of these issues in the normal as well as in the traumatized brain is essential in developing new treatment strategies. These issues also play a key role in interpreting data collected from monitoring techniques such as cerebral tissue PO2, jugular bulb oxygen saturation (SjvO2), near infra red spectroscopy (NIRS), microdialysis, intracranial pressure monitoring (ICP), laser Doppler flowmetry, and transcranial Doppler flowmetry--both in the experimental and in the clinical setting.
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Repetitive traumatic brain injury (TBI) occurs in a significant portion of trauma patients, especially in specific populations, such as child abuse victims or athletes involved in contact sports (e.g. boxing, football, hockey, and soccer). A continually emerging hypothesis is that repeated mild injuries may cause cumulative damage to the brain, resulting in long-term cognitive dysfunction. The growing attention to this hypothesis is reflected in several recent experimental studies of repeated mild TBI in vivo. ⋯ Additionally, it will be crucial to design and utilize proper controls, which can be more challenging than experimental approaches to single mild TBI. It will also be essential to combine, and compare, data derived from in vitro experiments with those conducted with animals in vivo. These issues, as well as a summary of findings from repeated TBI research, are discussed in this review.