Articles: brain-injuries.
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Acta Neurochir. Suppl. · Jan 1998
Interhemispheric pressure gradients in severe head trauma in humans.
Interhemispheric pressure gradients may occur following severe head trauma in patients even in the absence of intracranial space occupying lesions. A higher ICP of the contralateral hemisphere may escape routine unilateral ICP monitoring. ⋯ According to our data with a limited number of patients, interhemispheric pressure gradients seem to occur in the initial posttraumatic phase in some patients, and they seem to resolve following adequate ICP treatment after several hours. Therefore, simultaneous bilateral ICP measurement may be warranted in the initial posttraumatic phase.
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It is usually defficult in clinical practice to establish factors affecting final outcome in patients suffering severe diffuse brain injury (SDBI), due to the absence of specific semiology. ⋯ Clinical evaluation, early CT findings, ICP values and their response to medical treatment and clinical complications were found to be related (p < 0.05) to final outcome (GOS).
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Ann Fr Anesth Reanim · Jan 1998
[-Secondary cerebral stress of systemic origin in children with severe craniocerebral injuries-].
To assess incidence of secondary brain insults of systemic origin (SBISOs) such as arterial hypotension, hypoxaemia, hypercarbia, and anaemia in severely head injured children; to assess their impact on mortality and morbidity in the short- and long-term. ⋯ Hypotension was associated with significant increase in mortality (x 3.6) in children with severe head injury. The consequences were worse when anaemia was associated.
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Journal of neurotrauma · Dec 1997
Effects of nalmefene, CG3703, tirilazad, or dopamine on cerebral blood flow, oxygen delivery, and electroencephalographic activity after traumatic brain injury and hemorrhage.
Hemorrhage after traumatic brain injury (TBI) in cats produces significant decreases in cerebral oxygen delivery (DcereO2) and electroencephalographic (EEG) activity. To determine whether effective treatments for the separate insults of TBI and hemorrhagic shock would also prove effective after the clinically relevant combination of the two, we measured the effects of a kappa-opiate antagonist (nalmefene), an inhibitor of lipid peroxidation (tirilazad), a thyrotropin-releasing hormone analog (CG3703), a clinically useful pressor agent (dopamine) or a saline placebo on cerebral blood flow (CBF), and EEG activity after TBI and mild hemorrhagic hypotension. Cats (n = 40, 8 per group) were anesthetized with 1.6% isoflurane in N2O:O2 (70:30) and prepared for fluid-percussion TBI and microsphere measurements of CBF. ⋯ DcereO2 was significantly less than baseline in the saline-, dopamine-, and tirilazad-treated groups at R60 and in the dopamine-, tirilazad-, and CG3703-treated groups at R120. EEG activity remained unchanged in the nalmefene-treated group but deteriorated significantly at R60 or R120 compared to baseline in the other groups. Nalmefene and CG3703 preserved the hyperemic response to hemodilution (otherwise antagonized by TBI), and nalmefene prevented the deterioration in DcereO2 and EEG activity that occurs after TBI and hemorrhage.
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Journal of neurosurgery · Dec 1997
Contribution of vasogenic and cellular edema to traumatic brain swelling measured by diffusion-weighted imaging.
The contribution of brain edema to brain swelling in cases of traumatic brain injury remains a critical problem. The authors believe that cellular edema, the result of complex neurotoxic events, is the major contributor to brain swelling and that vasogenic edema, secondary to blood-brain barrier compromise, may be overemphasized. The objective of this study, therefore, was to quantify temporal water content changes and document the type of edema that forms during the acute and late stages of edema development following closed head injury (CHI). ⋯ This transient increase, however, was followed by a continuing decrease in ADC that began 40 to 60 minutes postinjury and reached a minimum value on Days 7 to 14 (10 +/- 3% reduction). Because the water content of the brain continued to increase during the first 24 hours postinjury (1.9 +/- 0.9%), it is suggested that the decreased ADC indicated cellular edema formation, which started to develop soon after injury and became dominant between 1 and 2 weeks postinjury. The study provides supportive evidence that cellular edema is the major contributor to posttraumatic swelling in diffuse CHI and defines the onset and duration of the increase in cellular volume.