Articles: brain-injuries.
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To present a normative database of hippocampal and temporal horn volume and to clarify the relationship between these measures and cognitive outcome in patients with traumatic brain injury. ⋯ Hippocampal and temporal horn volumes appear to be independent variables in healthy control subjects. Traumatic brain injury results in significant hippocampal atrophy and temporal horn enlargement. The hippocampus and temporal horn volumes were inversely correlated in the group with traumatic brain injury, suggesting a differential relationship of these structures in patients with brain injury as compared with control subjects. In the subacute phase, the volume of the temporal horn may be indicative of intellectual outcome and that of the hippocampus appears to be indicative of verbal memory function.
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Comparative Study
Treatment of refractory intracranial hypertension in severe traumatic brain injury with repetitive hypertonic/hyperoncotic infusions.
Rapid resuscitation of clinical and experimental traumatic brain injury (TBI) with hypertonic saline (HS) has been shown to improve neurological function and decrease intracranial pressure (ICP). The purpose of the present study was to test the efficacy of administration of HS (7.5%) combined with 6% hydroxyethyl starch (molecular weight 200,000/0.60-0.66; HHES) for the treatment of intracranial hypertension refractory to standard therapy in patients with severe TBI. With approval of the Institutional Ethics Committee six consecutive patients with severe TBI (GCS < 8) between 22 and 47 years of age (mean 32) who met the inclusion criteria (therapy resistant ICP > 25 mmHg, cerebral perfusion pressure (CPP) < 60 mmHg, plasma-Na+ < 150 mOsm and > 4 hours since the last HS/HHES treatment) were prospectively enrolled in the study. ⋯ Plasma sodium normalized within 30 min. HS/HES might become an interesting addition to conventional treatment maneuvers currently used for ICP therapy. It reduces otherwise therapy-resistant intracranial hypertension without negatively affecting blood pressure, blood gases and cerebral perfusion.
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Ann Fr Anesth Reanim · Jan 1997
Review[Treatment of intracranial hypertension in the case of severe craniocerebral injuries].
More than 50% of severely head-injured patients develop increased intracranial pressure, risking exacerbating ischaemic insults to the already injured brain. In approximately 10% of these cases, intracranial pressure may become unresponsive to medical or surgical treatment, with a resulting mortality of over 90%. ⋯ Recently, an algorithm for treating intracranial hypertension under three different therapeutic situations has been suggested, based on the successive application of effective agents with increasing associated risks. Therapeutic modalities of this protocol are discussed.
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Acta Neurochir. Suppl. · Jan 1997
Comparative StudyBlood-brain barrier breakdown occurs early after traumatic brain injury and is not related to white blood cell adherence.
The time course of blood-brain barrier (BBB) breakdown after traumatic brain injury (TBI) has important implications for therapy. This study was conducted in order to test post-traumatic BBB dysfunction in a model of fluid-percussion induced TBI in rabbits at 1 and 6 hours after TBI and relate it to white blood cell (WBC) activation. Ten anesthetized rabbits had chronic cranial windows implanted three weeks prior to experimentation. ⋯ We conclude that after fluid-percussion injury the BBB is damaged at 1 h post-trauma and that its function is restored 6 h later. Increased WBC sticking at 6 h is not associated with BBB breakdown. Whether WBCs may cause vascular permeability changes at a later point needs further investigation.