Journal of neurotrauma
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Journal of neurotrauma · Oct 2006
Practice GuidelineGuidelines for the pharmacologic treatment of neurobehavioral sequelae of traumatic brain injury.
There is currently a lack of evidence-based guidelines to guide the pharmacological treatment of neurobehavioral problems that commonly occur after traumatic brain injury (TBI). It was our objective to review the current literature on the pharmacological treatment of neurobehavioral problems after traumatic brain injury in three key areas: aggression, cognitive disorders, and affective disorders/anxiety/ psychosis. Three panels of leading researchers in the field of brain injury were formed to review the current literature on pharmacological treatment for TBI sequelae in the topic areas of affective/anxiety/ psychotic disorders, cognitive disorders, and aggression. ⋯ Options were recommended in the treatment of depression, bipolar disorder/mania, psychosis, aggression, general cognitive functions, and deficits in attention, speed of processing, and memory after TBI. The evidence-based guidelines and options established by this working group may help to guide the pharmacological treatment of the person experiencing neurobehavioral sequelae following TBI. There is a clear need for well-designed randomized controlled trials in the treatment of these common problems after TBI in order to establish definitive treatment standards for this patient population.
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Journal of neurotrauma · Oct 2006
Aspects on decompressive craniectomy in patients with traumatic head injuries.
In patients with traumatic brain injury (TBI), intracranial hypertension secondary to cerebral edema is a major problem. A last-tier treatment in these cases is decompressive craniectomy. The aim of the present retrospective investigation was to (1) study the long-time outcome in patients with traumatic head injuries with intracranial hypertension treated with decompressive craniectomy; (2) examine the effects on intracranial pressure (ICP) by the craniectomy; and (3) investigate the possible relationship between the size of the removed bone-flap and the effects on ICP. ⋯ The outcome of all patients could be assessed. The survival rate was 89%. Two patients died (both day 4 after the trauma); 68% of the patients had a favorable outcome (Glasgow Outcome Scale [GOS] score of 4 or 5); 16% were severely disabled (GOS score of 3); and one patient (5%) was left in a vegetative state.
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Journal of neurotrauma · Oct 2006
Diffusion tensor imaging in the corpus callosum in children after moderate to severe traumatic brain injury.
Diffusion tensor imaging (DTI) is a recent imaging technique that assesses the microstructure of the cerebral white matter (WM) based on anisotropic diffusion (i.e., water molecules move faster in parallel to nerve fibers than perpendicular to them). Fractional anisotropy (FA), which ranges from 0 to 1.0, increases with myelination of WM tracts and is sensitive to diffuse axonal injury (DAI) in adults with traumatic brain injury (TBI). However, previous DTI studies of pediatric TBI were case reports without detailed outcome measures. ⋯ In the TBI patients, higher FA was related to better functional outcome as measured by the dichotomized Glasgow Outcome Scale (GOS). FA also increased as a function of the area of specific regions of the corpus callosum such as the genu and splenium, and FA in the splenium was reduced with greater volume of lesions in this region. DTI may be useful in identifying biomarkers related to DAI and outcome of TBI in children.
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Journal of neurotrauma · Oct 2006
Traumatic brain injury produces delay-dependent memory impairment in rats.
Memory impairment following traumatic brain injury (TBI) is common in both humans and animals. A noteworthy feature of memory dysfunction in human TBI is impaired memory performance that is dependent on the delay between initial learning and recall of information. However, previous studies of TBI-induced memory impairment in animals have failed to control for the initial amount of learning between sham and injured animals. ⋯ However, as the delay increased to 30 and 120 sec, the performance of the injured animals deteriorated (p < 0.05). These results indicate that LFP injury produces delay-dependent memory impairments in rats. This is therefore a valid model of an important feature of memory impairment in human TBI, and should be a useful addition to the available methods for assessing memory impairment and the effect of therapeutic interventions after TBI.