Articles: brain-injuries.
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Review Comparative Study
Cellular and molecular correlates to plasticity during recovery from injury in the developing mammalian brain.
In summary, our studies indicate that the perinatal mammalian brain shows considerable plasticity in response to trauma. Studies carried out both in vivo in the perinatal mouse brain and in vitro in cell line culture and organotypic slice cultures of developing brain tissue, indicate that the cytokine, interleukin-1 beta (IL-1 beta) regulates early healing responses that restore the integrity of the damaged structure and create conditions conducive to the sprouting of new connections involved in plasticity. In response to a lesion placed in the cerebral cortex in a late third trimester embryo, astrocytes form a line that delimits damaged tissue being removed by phagocytic macrophages from tissue that will remain part of the neural parenchyma. ⋯ Similar sprouting occurred in vitro in organotypic slice culture of deafferented hippocampus. In culture, sprouting was first observed at the time of onset of astrocyte hypertrophy, indicating that astrocyte derived factors may play a role in regulating circuit reorganization. Viewed together, in vivo and in vitro studies indicate that IL-1 beta upregulation in neural tissue correlates with glial activities that underlie rapid healing and repair in the perinatal brain, and that glial activities associated with deafferentation may play a role in inducing compensatory neurite sprouting and cicuit reorganization.
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Acta neurochirurgica · Jan 1996
Randomized Controlled Trial Comparative Study Clinical TrialKetamine for analgosedative therapy in intensive care treatment of head-injured patients.
Ketamine was supposed to be contra-indicated in head injured patients although it possesses numerous advantages over other commonly used analgosedative drugs. Referring to these potential advantages and the lack of definitive data about its effect upon ICP, CPP or neurological development, we conducted a prospective study in which moderate or severely head injured patients (n = 35) were prospectively allocated to receive treatment either with a combination of ketamine or midazolam or fentanyl and midazolam. The initial dose was 6.5 mg/kg/day midazolam, 65 mg/kg/day ketamine or 65 micrograms/kg/day fentanyl and was later adjusted due to clinical requirements for a period of 3 to 14 days. ⋯ A comparison of the remaining patients revealed a lower requirement of catecholamines (significant on first day, p<0.05), an on average 8 mm Hg higher cerebral perfusion pressure and a 2 mm Hg higher intracranial pressure in the study [corrected] group. Enteral food intake was better in the study group. The outcome was comparable in both groups with or without inclusion of withdrawn patients.
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J Craniomaxillofac Trauma · Jan 1996
ReviewAvoiding secondary brain injury after severe head trauma: monitoring and management.
Research has demonstrated that much of the mortality and morbidity in severely head-injured patients is due to secondary injury. The development of techniques to monitor cerebral blood flow, arteriovenous difference of oxygen or saturation of jugular venous blood flow with oxygen, and cerebral metabolic rate of oxygen has led to recognition, treatment, and prevention of secondary insults. ⋯ Special emphasis is given to the factors governing both cerebral blood flow and cerebral blood volume, and how these factors can be monitored and manipulated to strike an optimal balance between the two. This information can aid in determining when it is safe to operate on patients with non-life-threatening conditions.
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J. Neuropathol. Exp. Neurol. · Jan 1996
Cytoskeletal derangements of cortical neuronal processes three hours after traumatic brain injury in rats: an immunofluorescence study.
Semiquantitative Western blot analyses have shown that traumatic brain injury (TBI) can produce significant loss of cytoskeletal proteins (neurofilament 68 [NF68], neurofilament 200 [NF200] and microtubule associated protein 2 [MAP2]) possibly by calpain-mediated proteolysis. Thus, we employed immunofluorescence (light and confocal microscopy) to study the histopathological correlates of acute neurofilament and MAP2 protein decreases observed 3 hours following unilateral cortical injury in rats. TBI induced dramatic alterations in NF68, NF200, and MAP2 immunolabeling in dendrites within and beyond contusion sites ipsilateral and contralateral to the injury site. ⋯ Acute axonal alterations detected with NF68 were minimal compared to immunofluorescence changes seen in dendritic regions. Therefore, preferential dendritic cytoskeletal derangements may be an early morphological feature of experimental traumatic brain injury in vivo. In addition, these cytoskeletal derangements may not be exclusively restricted to sites of contusion and cell death.
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Journal of neurosurgery · Jan 1996
Characterization of edema by diffusion-weighted imaging in experimental traumatic brain injury.
The objective of this study was to use diffusion-weighted magnetic resonance imaging (DWI) to help detect the type of edema that develops after experimental trauma and trauma coupled with hypotension and hypoxia (THH). Reduction in the apparent diffusion coefficients (ADCs) is thought to represent cytotoxic edema. In a preliminary series of experiments, the infusion edema model and middle cerebral artery occlusion models were used to confirm the direction of ADC change in response to purely extracellular and cytotoxic edema, respectively. ⋯ In the trauma alone group, the rise in ICP reached a maximum value (28 +/- 3 mm Hg) at 30 minutes with a significant and sustained increase in CBF despite a gradual decrease in CPP. The ADCs in this group were not significantly reduced. The data lead the authors to suggest that the rise in ICP following severe trauma coupled with secondary insult in this model is predominately caused by cytotoxic edema and that ischemia plays a major role in the development of brain edema after head injury.