Journal of neurotrauma
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Journal of neurotrauma · Jun 2001
Clinical TrialValidity and sensitivity to change of the extended Glasgow Outcome Scale in mild to moderate traumatic brain injury.
Using a structured outcome interview, this study addressed the validity and sensitivity to change of the Glasgow Outcome Scale (GOS) and the Extended GOS (GOSE) in a prospective study of patients who sustained mild (n = 30) to moderate (n = 13) traumatic brain injury (TBI) or general trauma (n = 44). The patients were recruited from the emergency center or inpatient units of Ben Taub General Hospital and invited to participate in follow-up examinations at 3 and 6 months. ⋯ Comparison of the 3-month outcome data disclosed that the GOSE and GOS scores did not differ for the TBI and general trauma groups. These findings lend further support for utilization of the GOSE in clinical trials when it is based on a structured interview.
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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 · May 2001
S-100 beta reflects the extent of injury and outcome, whereas neuronal specific enolase is a better indicator of neuroinflammation in patients with severe traumatic brain injury.
It has been hypothesized that immunoactivation may contribute to brain damage and affect outcome after traumatic brain injury (TBI). In order to determine the role of inflammation after TBI, we studied the interrelationship of the immune mediators sICAM-1 and IL-6 with the levels of S-100beta and neuronal specific enolase (NSE), both recognized markers of brain damage. In addition, the extent and type of cerebral injury and the neurological outcome were related to these measured markers of injury. ⋯ The contusion sizes assessed on the CT scans correlated with the means of S-100beta (r = 0.63, p < 0.05) and NSE (r = 0.71, p < 0.05) in CSF and with the mean of S-100beta in serum, although not statistically significant (r = 0.52, p = 0.06), but not with serum NSE. Interestingly, linear regression analysis demonstrated that means of S-100beta in CSF (r = 0.78, p = 0.002) and serum (r = 0.82, p < 0.001) correlated with the GOS. These results indicate that the elevation of these parameters in CSF depends on the extent of injury and that S-100beta may be a predictor of outcome after TBI, whereas NSE reflects better the inflammatory response.
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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.