Journal of neurotrauma
-
Journal of neurotrauma · Aug 1997
ReviewTransplant therapy: recovery of function after spinal cord injury.
Spinal cord injuries (SCI) result in devastating loss of function and altered sensation. Presently, victims of SCI have few remedies for the loss of motor function and the altered sensation often experienced subsequent to the injury. A goal in SCI research is to improve function in both acute and chronic injuries. ⋯ New recent work describing the in vitro propagation and characterization of human fetal spinal cord multipotential progenitor cells are also described in the context of a potential resource for transplantable cells. Additionally, data from transplantation experiments of human FSC cells into nonimmunosuppressed rat spinal cord are described, and the resultant improvements in behavioral outcome reported. Lastly, directions for future SCI research are proposed.
-
Spinal cord injury (SCI) frequently results in dysesthesias that have remained refractory to clinical treatments despite a variety of interventions. The failure of therapeutic strategies to treat dysesthesias after SCI is due to the lack of attention given to mechanisms that elicit chronic pain following SCI. An overview of the literature with respect to the development of chronic pain in the SCI patient population will be given. ⋯ The data presented support the development of central sensitization of dorsal horn neurons after spinal cord hemisection. This provides a mechanism for the development of mechanical and thermal allodynia after SCI. Hypotheses that account for the development of the central pain state after SCI, as well as therapeutic interventions to ameliorate the pain state, are discussed.
-
Journal of neurotrauma · Aug 1997
Cholinergic modulation of cerebral cortical blood flow changes induced by trauma.
These experiments tested the role of cholinergic mechanisms in the changes of cerebral cortical blood flow (CBF) induced by brain trauma. CBF was measured with Iodo-14C-antipyrine autoradiography, in 128 cerebral cortex regions of both hemispheres, distributed in eight coronal slices. The effects of a 6.3-mm diameter craniotomy over the left motor-sensory cortex with no weight drop, and of trauma (drop weight of 20 g from 30 cm height on left motor-sensory cortex through a 6.3 mm circular craniotomy) on CBF were studied at 2 and 24 h after the interventions. ⋯ The cerebral cortex contralateral to the trauma showed significantly higher CBF 24 h after trauma when compared to intact controls or craniotomy that peaked at the area symmetrical to the center of trauma. This phenomenon was also enhanced by physostigmine and completely blocked by scopolamine. These results suggest a prominent role of cholinergic mechanisms in the vascular adjustments that accompany cerebral trauma.
-
Journal of neurotrauma · Jul 1997
Interleukin-6 and interleukin-10 in cerebrospinal fluid after severe traumatic brain injury in children.
Cytokines may play an important role in the pathophysiology of traumatic brain injury (TBI) in children. Interleukin-6 (IL-6) is a proinflammatory cyotkine that plays a role in regenerative processes within the central nervous system (CNS), whereas interleukin-10 (IL-10) is an antiinflammatory cytokine. Both have been measured in serum and cerebrospinal fluid (CSF) as an index of the degree of inflammation in diseases, including sepsis and meningitis. ⋯ Increased IL-10 concentrations were independently associated with age < 4 years and mortality (p = 0.004 and 0.04, respectively, multivariate linear model). This study demonstrates that IL-6 is increased after TBI in children to levels similar to those reported in adults and is the first to show that IL-10 is increased in CSF of humans after TBI. These data suggest that there may be an age-dependent production of IL-10 after TBI in children.
-
Journal of neurotrauma · Jun 1997
Immunohistochemical study of calpain-mediated breakdown products to alpha-spectrin following controlled cortical impact injury in the rat.
This study examined the effect of unilateral controlled cortical impact on the appearance of calpain-mediated alpha-spectrin breakdown products (BDPs) in the rat cortex and hippocampus at various times following injury. Coronal sections were taken from animals at 15 min, 1 h, 3 h, 6 h, and 24 h after injury and immunolabeled with an antibody that recognizes calpain-mediated BDPs to alpha-spectrin (Roberts-Lewis et al., 1994). Sections from a separate group of rats were also taken at the same times and stained with hematoxylin and eosin. ⋯ The presence of BDPs to alpha-spectrin in the cortex at the site of impact, and in the rostral and contralateral cortex, coincided with morphopathology detected by hematoxylin and eosin. alpha-Spectrin BDPs were also observed in the hippocampus ipsilateral to the injury in the absence of overt cell death. This investigation provides further evidence that calpain is activated after controlled cortical impact and could contribute to necrosis at the site of injury. The appearance of calpain-mediated BDPs at sites distal to the contusion site and in the hippocampus also suggests that calpain activation may precede and/or occur in the absence of extensive morphopathological changes.