Articles: brain-injuries.
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Intensive care medicine · May 1999
Comparative StudyEarly SjvO2 monitoring in patients with severe brain trauma.
To investigate early cerebral variables after minimal resuscitation and to compare the adequacy of a cerebral perfusion pressure (CPP) guideline above 70 mmHg, with jugular bulb venous oxygen saturation (SjvO2) monitoring in a patient with traumatic brain injury (TBI). ⋯ The present study shows that early cerebral monitoring with SjvO2 is critical to assess cerebral ischemic risk and that MAP monitoring alone is not sensitive enough to determine the state of oxygenation of the brain. SjvO2 monitoring permits the early identification of patients with low CPP and high risk of cerebral ischemia. In emergency situations it can be used alone when ICP monitoring is contraindicated or not readily available. However, ICP monitoring gives complementary information necessary to adapt treatment.
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J. Neurol. Neurosurg. Psychiatr. · May 1999
Critical closing pressure in cerebrovascular circulation.
Cerebral critical closing pressure (CCP) has been defined as an arterial pressure threshold below which arterial vessels collapse. Hypothetically this is equal to intracranial pressure (ICP) plus the contribution from the active tone of cerebral arterial smooth muscle. The correlation of CCP with ICP, cerebral autoregulation, and other clinical and haemodynamic modalities in patients with head injury was evaluated. ⋯ Critical closing pressure, although sensitive to variations in ICP and CPP, cannot be used as an accurate estimator of these modalities with acceptable confidence intervals. The difference CCP-ICP significantly correlates with cerebral autoregulation, but it lacks the power to predict outcome after head injury.
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To demonstrate risk factors involved in the origin of late posttraumatic seizures (LPTSs) in civilian traumatic brain injury (TBI) rehabilitation patients and the occurrence of LPTSs in this population, as well as the time of the first late seizures, and influence of these seizures on functional and occupational long-term outcome. ⋯ Young children are more prone to early seizures, and adolescents and adults, to late seizures. The main risk factors for LPTSs are early seizures and depressed skull fracture. Severity of brain injury, as measured by a low GCS score, prolonged unconsciousness, and posttraumatic amnesia (PTA) without local brain lesion, should not be considered risk factor for LPTSs. Thorough follow-up of patients with TBI with seizures and adequate antiepileptic therapy may help attain rehabilitation goals and reemployment.
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Anesteziol Reanimatol · May 1999
Comparative Study[Clinico-pathogenetic variants of DIC syndrome in patients with severe craniocerebral trauma].
Detection of clinical and pathogenetic variants of the DIC syndrome for development of its differentiated therapy in multiple-modality treatment of severe craniocerebral injury was the purpose of this study. A total of 170 patients with grave craniocerebral injury were examined. The hemostasis system was studied by the following methods: analysis of platelet hemostasis, general coagulation tests, fibrinolysis evaluation, detection of physiological anticoagulants and markers of intravascular blood coagulation and fibrinolysis. Based on the clinical (intra- and extracranial) symptoms and results of studies of the hemostasis system, 3 clinical pathogenetic variants of the DIC syndrome were distinguished, which should be borne in mine when treating patients with severe craniocerebral injury developing the DIC syndrome.
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Journal of neurochemistry · May 1999
Effects of moderate hypothermia on constitutive and inducible nitric oxide synthase activities after traumatic brain injury in the rat.
We investigated the effects of therapeutic hypothermia (30 degrees C) on alterations in constitutive (cNOS) and inducible (iNOS) nitric oxide synthase activities following traumatic brain injury (TBI). Male Sprague-Dawley rats were anesthetized with 0.5% halothane and underwent moderate (1.8-2.2 atm) parasagittal fluid-percussion (F-P) brain injury. In normothermic rats (37 degrees C) the enzymatic activity of cNOS was significantly increased at 5 min within the injured cerebral cortex compared with contralateral values (286.5+/-68.9% of contralateral value; mean+/-SEM). ⋯ Posttraumatic hypothermia also significantly reduced iNOS activity at 7 days compared with normothermic rats (0.021+/-0.06 and 0.23+/-0.06 pmol/mg of protein/min, respectively; p < 0.05). The present results indicate that hypothermia (a) decreases early cNOS activation after TBI, (b) preserves cNOS activity at later periods, and (c) prevents the delayed induction of iNOS. Temperature-dependent alterations in cNOS and iNOS enzymatic activities may participate in the neuroprotective effect of hypothermia in this TBI model.