Journal of neurotrauma
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Journal of neurotrauma · Jul 2006
Comparative StudyEffect of early and delayed decompressive craniectomy on secondary brain damage after controlled cortical impact in mice.
The timing of decompressive craniectomy for the treatment of increased intracranial pressure (ICP) after traumatic brain injury (TBI) is a widely discussed clinical issue. Although we showed recently that early decompression is beneficial following experimental TBI, it remains unclear to what degree decompression craniectomy reduces secondary brain damage and if craniectomy is still beneficial when it is delayed by several hours as often inevitable during daily clinical practice. The aim of the current study was therefore to investigate the influence of craniectomy on secondary contusion expansion and brain edema formation and to determine the therapeutic window of craniectomy. ⋯ The beneficial effect of craniectomy was still present even when treatment was delayed by up to 3 h after trauma (p < 0.05). The current study clearly demonstrates that early craniectomy prevents secondary brain damage and significantly reduces brain edema formation after experimental TBI. Evaluation of early craniectomy as a therapeutic option after TBI in humans may therefore be indicated.
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Traumatic brain injury (TBI) has been associated with intravascular coagulation, which may be a result of thromboplastin released following brain injury. Clots thus formed are lysed by plasmin, which is activated by tissue-type and urokinase-type plasminogen activators (uPA). To evaluate the association between traumatic intravascular coagulation and post-traumatic outcome, uPA knockout (uPA-/-) transgenic mice (n=12) or wild-type littermates (WT; n=12) were anesthetized and subjected to controlled cortical impact (CCI) brain injury. ⋯ There was no significant difference in post-injury cognitive function between uPA-/- mice and WT mice. However, at 2 weeks post-injury, the brain-injured uPA-/- had a significantly larger volume of cortical tissue loss than their WT counterparts (p<0.05). These results demonstrate that the absence of uPA in mice aggravates acute motor deficit and exacerbates cortical tissue loss following CCI brain injury, and suggests a neuroprotective role of the fibrinolytic process following TBI.
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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
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 · 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.