Journal of neurotrauma
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Journal of neurotrauma · May 2001
Neuron-specific enolase serum levels after controlled cortical impact injury in the rat.
The aim of this study was to investigate the time course and the correlation of neuron-specific enolase (NSE) serum levels to the severity of traumatic brain injury in rats. Sixty-five male Wistar rats were subjected to severe cortical impact injury (100 PSI, 2 mm deformation). Blood samples were drawn directly after trauma and after 1, 6, 12, 24, and 48 h in the trauma group. ⋯ The highest NSE serum values were detected 6 h after trauma (31.5 microg/L mean, n = 10). In addition, we found a close relationship between NSE serum levels and the severity of traumatic brain injury in the cortical impact model. NSE serum levels reflect in a time-dependent manner the severity of brain trauma induced by cortical impact model in rat.
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Journal of neurotrauma · Apr 2001
Reduction of pathological and behavioral deficits following spinal cord contusion injury with the selective cyclooxygenase-2 inhibitor NS-398.
Spinal cord injury (SCI) results in loss of locomotor function and development of abnormal chronic pain syndromes (mechanical allodynia, thermal hyperalgesia). Following injury, secondary mechanisms including release of excitatory amino acids, inflammation and lipid peroxidation damage neural cells through release of cytotoxic free radicals. We hypothesized that selective inhibition of cyclooxygenase-2 (COX-2), an inducible inflammatory mediator, would decrease tissue damage and subsequently reduce locomotor deficits and development of chronic central pain syndromes after injury. ⋯ Histological examination of spinal segments at the lesion segment demonstrated reduced lesion extent and increased viable tissue when compared to vehicle controls. Prostaglandin E2 levels were significantly lowered in NS-398-treated but not vehicle-treated animals 12 h after injury. These results support the role of COX-2 in reducing pathological and behavioral deficits after spinal cord injury.
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Journal of neurotrauma · Apr 2001
Cellular inflammatory response associated with breakdown of the blood-brain barrier after closed head injury in rats.
This study reports a widespread microglial response characterized by an upregulation of surface antigens, such as complement type 3 receptors (CR3) and major histocompatibility complex (MHC) class II antigens on these cells following closed head injury. Increased expression of CR3 (OX-42) and MHC class II antigens (OX-6) was observed in rats killed at 1, 3, and 5 days after injury. Intense OX-42 immunoreactivity was observed in microglial cells throughout the brain with a smaller number of them being OX-6 positive. ⋯ In the latter, it is conceivable that the ensuing leakage of plasma immunoglobulins and other serum-derived materials could induce the expression of MHC class II antigens on microglia. The mechanism causing the BBB dysfunction is not clear, although present results suggest that excessive release of nitric oxide (NO) may be a contributory factor. The widespread activation of microglia in rats after head injury suggests their involvement in increased endocytosis and immunological responses.
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Journal of neurotrauma · Apr 2001
Differential cellular accumulation of connective tissue growth factor defines a subset of reactive astrocytes, invading fibroblasts, and endothelial cells following central nervous system injury in rats and humans.
In brain injury, the primary trauma is followed by a cascade of cellular and molecular mechanisms resulting in secondary injury and scar formation. Astrogliosis and expression of transforming growth factor beta (TGF-beta) are key components of scar formation. A cytokine mediating the effects of TGF-beta is connective tissue growth factor (CTGF), a fibrogenic peptide encoded by an immediate early gene with suggested roles in tissue regeneration and aberrant deposition of extracellular matrix. ⋯ The restricted accumulation of CTGF+-reactive astrocytes and CTGF+ fibroblastoid cells lining the adjacent laminin+ basal lamina suggests participation of these cells in scar formation. Furthermore, peri-lesional upregulation of endothelial CTGF expression points to a role in blood-brain barrier function and angiogenesis. In addition, CTGF appears to be a sensitive marker of early astrocyte activation.
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Journal of neurotrauma · Feb 2001
The relation between acute physiological variables and outcome on the Glasgow Outcome Scale and Disability Rating Scale following severe traumatic brain injury.
The relation between outcome and duration of adverse physiological events was studied, using suggested critical physiological values. Subjects were 184 patients with severe traumatic brain injury who received continuous monitoring of intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP), and jugular venous oxygen saturation. ⋯ When analyses excluded patients who died, the relation between adverse physiological events and GOS was nonsignificant; however, duration of ICP, MAP, and CPP still accounted for a significant portion of the variance in DRS scalres. The relative sensitivity of the GOS and DRS is discussed.