Journal of neurotrauma
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Journal of neurotrauma · Jun 2006
Neurobehavioral and quality of life changes associated with growth hormone insufficiency after complicated mild, moderate, or severe traumatic brain injury.
Adult-onset growth hormone deficiency (GHD) has been associated with reduced quality of life (QOL) and neurobehavioral (NB) deficits. This prospective study tested the hypothesis that traumatic brain injury (TBI) patients with GHD or GH insufficiency (GHI) would exhibit greater NB/QOL impairment than patients without GHD/GHI. Complicated mild, moderate, and severe adult TBI patients (GCS score 3-14) had pituitary function and NB/QOL testing performed 6-9 months postinjury. ⋯ At 6-9 months postinjury, patients with GHD/GHI had higher rates of at least one marker of depression (p<0.01), and reduced QOL (by SF-36 Health Survey) in the domains of limitations due to physical health (p=0.02), energy and fatigue (p=0.05), emotional well-being (p=0.02), pain (p=0.01), and general health (p=0.05). Chronic GHI develops in approximately 18% of patients with complicated mild, moderate, or severe TBI, and is associated with depression and diminished QOL. The impact of GH replacement therapy on NB function and QOL in these TBI patients is being tested in a randomized placebo-controlled trial.
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Journal of neurotrauma · Jun 2006
Dural repair reduces connective tissue scar invasion and cystic cavity formation after acute spinal cord laceration injury in adult rats.
This study examined whether duraplasty after acute cervical laceration spinal cord injury (SCI) in a rat model could (1) improve cerebrospinal fluid (CSF) circulation adjacent to the injury; (2) minimize connective tissue scarring; and (3) reduce post-traumatic inflammation and cystic cavitation. Following a transverse dural/arachnoid incision and C5-6 dorsal spinal hemisection, a 5-mm2 cadaveric dura mater allograft was placed over the lesion and fixed with fibrin glue (n=12). Control animals received an identical dural/arachnoid incision and cervical dorsal hemisection without dural repair (n=12). ⋯ Stereological analysis demonstrated that duraplasty resulted in a significant reduction in lesion volume at each time-point (p<0.01) associated with a nearly complete attenuation of post-traumatic cystic cavitation (p<0.001). Immunofluorescence studies demonstrated that duraplasty reduced the infiltration of ED-1-positive macrophages/microglia into and surrounding the lesion site, which may be responsible for the marked reduction in secondary injury following duraplasty. We conclude that duraplasty following acute spinal cord laceration may (1) improve CSF flow by limiting meningeal fibrosis; (2) reduce connective tissue scar formation; and (3) attenuate macrophage accumulation and progressive secondary injury.
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Journal of neurotrauma · Jun 2006
Intrathecal and systemic concentration of NT-proBNP in patients with severe traumatic brain injury.
Outcome of patients suffering from traumatic brain injury (TBI) depends on the development of secondary brain damage. In this context, recent studies underlined the role of the natriuretic peptides- atrial natriuretic peptide and brain natriuretic peptide (BNP)-in aneurysmatic subarachnoidal hemorrhage (SAH). Especially BNP correlates with intracranial pressure and clinical outcome after SAH. ⋯ For the first time, we evaluated intrathecal and systemic NT-proBNP concentrations in patients suffering from severe TBI. Interestingly, NT-proBNP in CSF and serum was significantly elevated in patients exhibiting an ICP of >15 mm Hg. Further studies are currently performed to elucidate the physiologic role of NT-proBNP in TBI.
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Journal of neurotrauma · May 2006
Inhibition of Fas-mediated apoptosis through administration of soluble Fas receptor improves functional outcome and reduces posttraumatic axonal degeneration after acute spinal cord injury.
Fas receptor activation has been implicated in inflammatory responses, programmed cell death, Wallerian degeneration in neural injury and the axotomy induced death of motoneurons. Recent work using transection models of spinal cord injury (SCI) demonstrated that neutralization of Fas ligand with antibodies may promote axonal regeneration and functional recovery. Moreover, recent studies from our laboratory in mutant mice with deficient expression of Fas, show reduced cell death and enhanced behavioural recovery after SCI. ⋯ An in vitro model of SCI demonstrated that sFasR administration decreases cell death as assessed by propidium iodide fluorescence. Furthermore, in a moderately severe in vivo clip compression model of SCI at C7-T1, we demonstrate that subarachnoid infusion of sFasR results in increased neuron and oligodendrocyte survival, improved tissue and long tract axonal preservation, reduced apoptotic cell death and enhanced functional neurological outcome after acute SCI. These results strongly suggest that inhibiting Fas receptor activation is neuroprotective after acute SCI and that this strategy may have important translational significance.
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Journal of neurotrauma · May 2006
Comparative StudyBasso Mouse Scale for locomotion detects differences in recovery after spinal cord injury in five common mouse strains.
Genetically engineered mice are used extensively to examine molecular responses to spinal cord injury (SCI). Inherent strain differences may confound behavioral outcomes; therefore, behavioral characterization of several strains after SCI is warranted. The Basso, Beattie, Bresnahan Locomotor Rating Scale (BBB) for rats has been widely used for SCI mice, but may not accurately reflect their unique recovery pattern. ⋯ BMS revealed significantly higher recovery in C57BL/10, B10. PL and F1 than the C57BL/6 and BALB/c strains after moderate SCI (p < 0.05). The differing behavioral response to SCI suggests inherent genetic factors significantly impact locomotor recovery and must be considered in studies with inbred or genetically engineered mouse strains.