Articles: brain-injuries.
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Journal of neurotrauma · Jul 1999
Clinical TrialTGF-beta is elevated in the CSF of patients with severe traumatic brain injuries and parallels blood-brain barrier function.
Traumatic brain injury (TBI) induces local and systemic immunologic changes, release of cytokines, and cell activation. Perpetuation of these cascades may contribute to secondary damage to the brain. Therefore, the ability of the antiinflammatory mediator transforming growth factor-beta (TGF-beta) to downregulate intrathecal immunoactivation may be of fundamental value for diminishing the incidence and extent of secondary insults. ⋯ Levels of TGF-beta could not be correlated with extent of initial injury by computed tomography (CT), CD4/CD8 ratios, acute lung injury, or clinical outcome as rated by the Glasgow Outcome Scale (GOS). Although increased levels of TGF-beta in CSF seem to parallel BBB function, a partial intrathecal production is suggested, possibly modulated by elevation of interleukin-6 (IL-6). Thus, TGF-beta may function as a factor in the complex cytokine network following TBI, acting as an antiinflammatory and neuroprotective mediator.
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Brain injury : [BI] · Jul 1999
ReviewCognitive and psychosocial outcome following moderate or severe traumatic brain injury.
The outcome of 96 consecutive adult patients with moderate to severe head injury was sequentially measured at 6, 12 and 24 months post-injury. In addition to global outcome using the Glasgow Outcome Scale (GOS) and a battery of neuropsychological tests of cognitive function, the Head Injury Symptom Checklist (HISC) and Relative's Questionnaire (RQ) were used. Although poorer GOS scores and severe cognitive impairments were typically associated with greater severity of initial injury, relatives reported similar functional problems irrespective of injury severity. This illustrates the legacy of moderate head injury in influencing many aspects of everyday life, supporting the argument that the needs of this group should not be overlooked.
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Neurological research · Jul 1999
ReviewIndomethacin: a review of its cerebral blood flow effects and potential use for controlling intracranial pressure in traumatic brain injury patients.
Traumatic brain injury (TBI) causes about 75,000 deaths and leaves approximately 200,000 people disabled in USA each year. Brain swelling and increased intracranial pressure (ICP) contribute to this morbidity and mortality. Aggressive management protocols, including ICP control, have been shown to reduce the overall mortality from 50% to 36% following severe head injury. ⋯ IND should only be considered an experimental treatment for control of refractory ICP in TBI patients. Larger, well-designed randomized trials in TBI patients will provide more efficacy and safety data and delineate the effects of IND alone or in combination with other proven, effective, or experimental therapies. Once these concerns have been addressed, larger outcome studies will ultimately be needed to determine the role of IND for ICP control in TBI patients.
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Sheng Li Ke Xue Jin Zhan · Jul 1999
Review[Neural and hemodynamic mechanisms of neurogenic pulmonary edema].
Acute pulmonary edema has been reported in man and animals with intracranial disorders, head trauma or cerebral compression. In anesthetized rats, cerebral compression produced acute, fulminating and fatal lung injury. ⋯ Pulmonary volume loading was the result of drastic decrease in aortic flow accompanying a decline in pulmonary arterial flow. The acute increase in pulmonary blood volume caused severe rises in pulmonary arterial and venous pressures leading to disruption of lung vessels.
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Critical care medicine · Jul 1999
Clinical Trial Controlled Clinical TrialThiopental attenuates energetic impairment but fails to normalize cerebrospinal fluid glutamate in brain-injured patients.
Brain-injured patients are susceptible to secondary brain damage related to decreased cerebral perfusion pressure associated with edema formation and increased intracranial pressure (ICP). Whenever conventional therapy fails to reduce elevated ICP, barbiturate coma represents an additional intervention that may control ICP. In patients suffering from severe traumatic brain injury, cerebrospinal fluid levels of glutamate, hypoxanthine, and lactate were measured during barbiturate coma and correlated to electroencephalographic recordings and ICP. ⋯ Barbiturate coma does not unequivocally preserve energetic stability despite successful suppression of neuronal activity. Despite the use of barbiturate coma in patients with refractory intracranial hypertension, persistent release or impaired uptake of glutamate may be associated with continuous anaerobic metabolism, as shown by increases in cerebrospinal fluid hypoxanthine and lactate levels.