Articles: brain-injuries.
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To identify early prognostic value of brain injury, a comparison was made between computerized tomography (CT) findings, coagulation abnormalities, and clinical features in 51 patients with closed head injury. The patients were divided into three groups according to their plasma level of fibrin-fibrinogen degradation product (FDP): normal group (FDP 10 micrograms/ml or less) in 20 patients; moderately abnormal group (FDP 10-40 micrograms/ml) in 15 patients; and highly abnormal group (FDP 40 micrograms/ ml or more) in 16 patients. Cases with a fatal clinical course were mostly associated with very high FDP level. ⋯ Although severe head injury (GCS 8 or less) was found in 44% of the highly abnormal group and 13% of the moderately abnormal group, normal group only had one case (5%). Very high FDP concentrations were found to be associated with combined hemorrhagic lesions and mass effect on CT scan, but not with a specific localization of brain damage. In summary, the evaluation of coagulation and fibrinolytic function in patients following closed head injury might have both diagnostic and prognostic value.
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Head traumas frequently occur in polytrauma patients but are also found as isolated injuries. In our hospital trauma center without a neurosurgical department, in a 21-month period, 489 patients with head/brain trauma were treated. This represents 6.5% of all patients treated in the trauma and reconstructive surgery clinic. ⋯ In patients with intracerebral bleeding, bleeding in the dorsal fossa, injury of brain nerves, carotid artery or sinus cavernosus injuries, frontobasal injuries with liquor fistula or pneumonencephalon, transfer of the patients to specialized neurosurgical centers is indicated. With this selection, we obtained the same results in a trauma center without a neurosurgical department as reported in the literature. This avoids overloading neurosurgical centers with head/brain injury patients.
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Journal of neurosurgery · Oct 1996
Moderate hypothermia in patients with severe head injury: cerebral and extracerebral effects.
Cerebral and extracerebral effects of moderate hypothermia (core temperature 32.5 degrees C-33.0 degrees C) were prospectively studied in 10 patients with severe closed head injury (Glasgow Coma Scale score < 7) in the intensive care unit of a university hospital. Hypothermia was induced by cooling the patient's body surface with water-circulating blankets. Before cooling, a conventional intracranial pressure (ICP) reduction therapy was applied, which remained unchanged throughout the study. ⋯ Seven patients made a good recovery; one survived severely disabled; and two patients died. Moderate hypothermia is effective in preventing secondary brain damage while reducing cerebral ischemia. However, there are potentially hazardous side effects that require additional monitoring.
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Comparative Study
Neuroprotection by propofol in acute mechanical injury: role of GABAergic inhibition.
1. Whole cell patch-clamp and extracellular field recordings were obtained from granule cells of the dentate gyrus in 400-microns-thick brain slices of the adult rat to determine the actions of the intravenous general anesthetic 2,6-diisopropylphenol (propofol) on acute neuronal survival and preservation of synaptic integrity after amputation of dendrites (dendrotomy), and to determine the role of gamma-aminobutyric acid-A (GABAA)-receptor-mediated inhibition in the neuroprotective effects of propofol. The actions of propofol were compared with those exerted by another widely used intravenous general anesthetic, 5-ethyl-5-[1-methylbutyl]-2-thiobarbituric acid (thiopental). 2. ⋯ The failure to rescue cells from dendrotomy-induced injury did not result from a decreased sensitivity of the GABAA receptors to the anesthetics, because the potentiating effects of the anesthetics on mIPSCs from control and dendrotomized neurons were not different. 7. These data indicate that propofol potentiates synaptic inhibition pre- and postsynaptically, and, when present during dendrotomy, it can protect neurons from acute mechanical-injury induced cell death via potentiation of GABAA receptor functions. However, propofol fails to provide neuroprotection against dendrotomy-induced changes in synaptic physiology.