Journal of neurotrauma
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Early investigations involving central nervous system (CNS) temperature lowering to protect against the detrimental effects of hypoxia and ischemia were based on the observation that hypothermia reduces brain metabolism and energy consumption. The protective effects of hypothermia have been demonstrated in numerous experimental models of cerebral ischemia and recently in models of brain trauma. These observations also led to the application of hypothermia, in the form of local spinal cord cooling (LSCC), in animal models of experimental spinal cord injury (SCI). ⋯ The application of the technique itself is fraught with difficulties. It requires acute surgery in a traumatized patient, a wide multilevel laminectomy, and minimizing the time interval between injury and the application of spinal cord cooling. Recent studies in experimental brain ischemia strongly suggest that a drastic lowering of CNS temperature may be unnecessary to lessen the degree of tissue damage occurring following an ischemic brain injury.(ABSTRACT TRUNCATED AT 250 WORDS)
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Journal of neurotrauma · May 1992
Randomized Controlled Trial Comparative Study Clinical TrialSystemic hypothermia in treatment of brain injury.
An extensive literature suggests that there are minimal complications of systemic hypothermia in humans at and above 30 degrees C for periods of several days. Intracranial hemorrhage has been found to complicate profound hypothermia (10-15 degrees C), and ventricular arrhythmias occur at temperatures below 30 degrees C. Our initial clinical studies were with 21 patients undergoing elective craniotomy cooled to 30-32 degrees C for 1-8 h (mean 4 h). ⋯ No intracranial hemorrhage or other complications were found. With surface cooling, intravascular temperature dropped at 1.6 degrees C/h. Based on the safety of surface cooling to a core temperature of 32 degrees C for 48 h, we are conducting a randomized study of this level of hypothermia in patients with severe brain injury, cooled within 6 h of injury.
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Journal of neurotrauma · Mar 1992
ReviewCerebral blood flow, cerebral blood volume, and cerebrovascular reactivity after severe head injury.
Traumatic brain injury (TBI) often causes disturbances of the cerebrovascular circulation, which contribute to the infliction of secondary injury, although the complex nature of the mechanisms involved is not fully understood. First, the role of ischemia in TBI is still controversial. Despite experimental and pathologic data suggesting important interactions between ischemia and trauma, evidence for posttraumatic ischemia with CBF measurements in patients so far had eluded most investigators. ⋯ Impairment of cerebrovascular CO2 reactivity and autoregulation often occurs after TBI. Although no correlation with the severity of injury or outcome has been established, it is obvious that diminished adaptive responses of the cerebral vasculature render the brain more vulnerable to additional systemic insults, such as derangements of blood pressure, altered rheology, or hypoxia. The posttraumatic status of vascular reactivity and autoregulation also has important implications with regard to the treatment of high ICP, in particular for the use of hyperventilation and pharmacologic management of blood pressure, which are discussed in detail.
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Journal of neurotrauma · Mar 1992
ReviewExperimental models for spinal cord injury research: physical and physiological considerations.
This paper describes historical and current experimental models used to develop our current understanding of the biomechanics and pathophysiology of traumatic spinal cord injury; the advantages and limitations of current experimental models; considerations for selecting an appropriate injury model based on experimental objectives; and key physiological factors in the spinal cord injury response that may interact with the injury response and alter the outcome. All of the above must be considered in the development and selection of an appropriate experimental injury model that meets specific needs. Various experimental models have been developed to study spinal cord injury and the pathophysiological and physical mechanisms responsible for tissue damage and loss of function. ⋯ Also, experimental techniques, especially anesthesia, and surgical procedures, should be carefully reviewed for interactions with the injury response or potential therapeutic interventions to ensure validity of interpretation. It is hoped that data correlating physical spinal cord injury parameters with functional outcome will ultimately be combined with data on vertebral injury and spinal failure mechanics to further our understanding of clinical injury. Such approaches should lead to interventions that reduce the incidence and severity of traumatic human spinal cord injury.