Progress in brain research
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Ischemia is a common problem after traumatic brain injury (TBI) that eludes detection with standard monitoring. In this review we will discuss four available techniques (SjVO2, PET, NIRS and PbrO2) to monitor cerebral oxygenation. We present technical data including strengths and weaknesses of these systems, information from clinical studies and formulate a vision for the future.
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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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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.
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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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Acute spinal cord injury (SCI) is a devastating neurological disorder that can affect any individual at a given instance. Current treatment options for SCI include the use of high dose methylprednisolone sodium succinate, a corticosteroid, surgical interventions to stabilize and decompress the spinal cord, intensive multisystem medical management, and rehabilitative care. ⋯ These include the Surgical Treatment for Acute Spinal Cord Injury Study (STASCIS) Trial to evaluate the role and timing of surgical decompression for acute SCI, neuroprotection with the semisynthetic second generation tetracycline derivative, minocycline; aiding axonal conduction with the potassium channel blockers, neuroregenerative/neuroprotective approaches with the Rho antagonist, Cethrin; the use of anti-NOGO monoclonal antibodies to augment plasticity and regeneration; as well as cell-mediated repair with stem cells, bone marrow stromal cells, and olfactory ensheathing cells. This review overviews the pathobiology of SCI and current treatment choices before focusing the rest of the discussion on the variety of promising neuroprotective and cell-based approaches that have recently moved, or are very close, to clinical testing.