Journal of neurotrauma
-
Journal of neurotrauma · Jul 2005
Pre-Injury magnesium treatment prevents traumatic brain injury-induced hippocampal ERK activation, neuronal loss, and cognitive dysfunction in the radial-arm maze test.
We studied the effect of pre-injury magnesium (Mg(2+)) treatment on hippocampal extracellular signal- regulated kinase (ERK) activation induced by lateral fluid-percussion (FP) brain injury, and on working and reference memory in the radial-arm maze test in rats subjected to such traumatic brain injury (TBI) (n = 56) or to sham injury (n = 12). In the ipsilateral hippocampus, an increase in the phospho-ERK level was detected at 10 min after injury in rats subjected to FP brain injury of moderate severity (1.9-2.0 atm) as compared to sham-injured controls (p < 0.01), and was maintained for at least 120 min after injury (p < 0.05). In the contralateral hippocampus, the phospho-ERK level was transiently increased at 10 min after injury but fell to nearly its basal level by 30 min. ⋯ Mg(2+) treatment also significantly prevented injury- induced neuronal loss in the ipsilateral hippocampus (p < 0.05 vs. vehicle-treated, brain-injured controls). At 2 weeks after injury, Mg2+ treatment was found to have significantly prevented injury-induced impairments in working (p < 0.0001 vs. vehicle-treated, brain-injured controls) and reference memory (p < 0.05) in the radial-arm maze test. The present study demonstrates that pretreatment with Mg(2+) prevents post-traumatic hippocampal ERK activation and neuronal loss, and cognitive dysfunction in the radial-arm maze test.
-
Journal of neurotrauma · Jun 2005
Randomized Controlled Trial Multicenter Study Comparative Study Clinical TrialEfficacy of standard trauma craniectomy for refractory intracranial hypertension with severe traumatic brain injury: a multicenter, prospective, randomized controlled study.
To compare the effect of standard trauma craniectomy (STC) versus limited craniectomy (LC) on the outcome of severe traumatic brain injury (TBI) with refractory intracranial hypertension, we conducted a study at five medical centers of 486 patients with severe TBI (Glasgow Coma Scale score = 8) and refractory intracranial hypertension. In all 486 cases, refractory intracranial hypertension, caused by unilateral massive frontotemporoparietal contusion, intracerebral/subdural hematoma, and brain edema, was confirmed on a CT scan. The patients were randomly divided into two groups, one of which underwent STC (n = 241) with a unilateral frontotemporoparietal bone flap (12 x 15 cm), and the second of which underwent LC (n = 245) with a routine temporoparietal bone flap (6 x 8 cm). ⋯ In addition to these findings, the incidence of delayed intracranial hematoma, incisional hernia, and CSF fistula was lower in the STC group than in the LC group (p < 0.05), although the incidence of acute encephalomyelocele, traumatic seizure, and intracranial infection was not significantly different in the two groups (p > 0.05). The results of the study indicate that STC significantly improves outcome in severe TBI with refractory intracranial hypertension resulting from unilateral frontotemporoparietal contusion with or without intracerebral or subdural hematoma. This suggests that STC, rather than LC, be recommended for such patients.
-
Journal of neurotrauma · Jun 2005
Histopathological and behavioral characterization of a novel cervical spinal cord displacement contusion injury in the rat.
Cervical contusive trauma accounts for the majority, of human spinal cord injury (SCI), yet experimental use of cervical contusion injury models has been limited. Considering that (1) the different ways of injuring the spinal cord (compression, contusion, and transection) induce very different processes of tissue damage and (2) the architecture of the spinal cord is not uniform, it is important to use a model that is more clinically applicable to human SCI. Therefore, in the current study we have developed a rat model of contusive, cervical SCI using the Electromagnetic Spinal Cord Injury Device (ESCID) developed at Ohio State University (OSU) to induce injury by spinal cord displacement. ⋯ Characterization of the model involved the analysis of the temporal histopathological progression of the injury over 9 weeks using histochemical stains to analyze white and gray mater integrity and immunohistochemistry to examine cellular changes and physiological responses within the injured spinal cord. Accompanying the histological analysis was a comprehensive determination of the behavioral functionality of the animals using a battery of motor tests. Characterization of this novel model is presented to enable and encourage its future use in the design and experimental testing of therapeutic strategies that may be used for human SCI.
-
Many survivors of head injury suffer chronic personality changes, such as increased impulsivity and a lack of insight and poor judgment. These changes are well recognized and likely to affect the ability to make decisions. However, systematic investigations into their nature have been limited. ⋯ Examination of the survivors' betting behavior revealed that they responded impulsively compared to controls. This pattern of prolonged decision making and poor quality of decisions is similar to that found in patients with orbitofrontal cortex lesions, whilst impulsive betting has been associated with abnormalities of the dopamine system. These complex deficits in decision making may contribute to difficulties with poor judgment and inhibition in head injury survivors.
-
Journal of neurotrauma · Jun 2005
Progesterone differentially regulates pro- and anti-apoptotic gene expression in cerebral cortex following traumatic brain injury in rats.
Although the administration of progesterone has been shown to be neuroprotective in experimental models of traumatic brain injury (TBI), the mechanisms for this beneficial effect are still poorly understood. The present study examined the effects of progesterone on mRNA and protein levels of the Bcl-2 apoptosis regulatory genes, bax, bad, bcl-2, and bcl-x(L), in cerebral cortex after TBI. Male Sprague-Dawley rats were subjected to either sham surgery or lateral fluid percussion brain injury of moderate severity (2.4-2.6 atm). ⋯ After TBI, progesterone treatment reduced bax and bad mRNA levels in the ipsilateral cerebral cortex of TBI rats, and decreased Bax and Bad protein levels. In addition, bcl-2 and bcl-x(L) mRNA levels, as well as Bcl-2 and Bcl-x(L) protein expression, were increased by progesterone in TBI injured cortex. These data indicate that one of the neuroprotective mechanisms of progesterone may be related to its differential regulation of apoptotic signals.