Journal of neurotrauma
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Journal of neurotrauma · Sep 2010
Comparative StudyCare of rats with complete high-thoracic spinal cord injury.
The complications of spinal cord injury (SCI) increase in number and severity with the level of injury. A recent survey of SCI researchers reveals that animal models of high SCI are essential. Despite this consensus, most laboratories continue to work with mid- or low-thoracic SCI. ⋯ Here we provide details of our animal care procedures, including acclimatization, housing, diet, antibiotic prophylaxis, surgical procedures, post-operative monitoring, and prevention of complications. In our laboratory, this comprehensive approach consistently produces good outcomes following T3 complete transection SCI: using body weight as an objective indicator of animal health, we have found that our rats typically return to pre-operative weights within 10 days of T3 complete SCI. It is our hope that the information provided here will improve care of experimental animals, and facilitate adoption of models that directly address the complications associated with higher level injuries.
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Journal of neurotrauma · Sep 2010
Comparative StudyAntagonism of R-type calcium channels significantly improves cerebral blood flow after subarachnoid hemorrhage in rats.
The effects of R-type calcium channels on cerebral blood flow (CBF) and vasospasm pathways following subarachnoid hemorrhage (SAH) have not been well studied. The aim of this study was to investigate the role of R-type calcium channels in vasospasm development and treatment. Sixty-five rats were randomly divided into four groups: sham (n = 14), SAH (n = 17), SAH + nimodipine (n = 17), and SAH + SNX-482 (n = 17). ⋯ Nimodipine had no significant effect on CBF reduction compared to the SAH group (p > 0.008), whereas SNX-482 significantly inhibited CBF reduction (p < 0.008). Both MLC2 phosphorylation and calponin degradation appeared to be inhibited by SNX-482, whereas the effects of nimodipine were relatively blunted. We concluded that an R-type calcium channel antagonist may improve CBF following SAH by partially inhibiting MLC2 phosphorylation and calponin degradation, and may exceed the potential of an L-type calcium channel antagonist, which suggests a more crucial role for R-type calcium channels in the development of SAH vasospasm and its treatment.
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Journal of neurotrauma · Sep 2010
Case ReportsSecond-impact syndrome and a small subdural hematoma: an uncommon catastrophic result of repetitive head injury with a characteristic imaging appearance.
There have been a handful of previously published cases of athletes who were still symptomatic from a prior head injury, and then suffered a second injury in which a thin, acute subdural hematoma (SDH) with unilateral hemisphere vascular engorgement was demonstrated on CT scan. In those cases, the cause of the brain swelling/dysautoregulation was ascribed to the presence of the acute SDH rather than to the acceleration/deceleration forces that caused the SDH. We believe that the brain swelling is due to "second-impact dysautoregulation," rather than due to the effect of the SDH on the underlying hemisphere. ⋯ The clinical history and the unique neuroimaging features of this entity on CT are described and illustrated in detail. The CT findings included an engorged cerebral hemisphere with initial preservation of grey-white matter differentiation, and abnormal mass effect and midline shift that appeared disproportionately greater than the size of the SDH. In addition, the imaging similarities between our patients and those with non-accidental head trauma (shaken-baby syndrome) will be discussed.
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Journal of neurotrauma · Aug 2010
Resting cerebral blood flow alterations in chronic traumatic brain injury: an arterial spin labeling perfusion FMRI study.
Non-invasive measurement of resting state cerebral blood flow (CBF) may reflect alterations of brain structure and function after traumatic brain injury (TBI). However, previous imaging studies of resting state brain in chronic TBI have been limited by several factors, including measurement in relative rather than absolute units, use of crude spatial registration methods, exclusion of subjects with substantial focal lesions, and exposure to ionizing radiation, which limits repeated assessments. This study aimed to overcome those obstacles by measuring absolute CBF with an arterial spin labeling perfusion fMRI technique, and using an image preprocessing protocol that is optimized for brains with mixed diffuse and focal injuries characteristic of moderate and severe TBI. ⋯ Hypoperfusion in superior and middle frontal cortices, in contrast, was associated with focal lesions. These results suggest that structural lesions, both focal and diffuse, are the main contributors to the absolute CBF alterations seen in chronic TBI, and that CBF may serve as a tool to assess functioning neuronal volume. We also speculate that resting reductions in posterior cingulate perfusion may reflect alterations in the default-mode network, and may contribute to the attentional deficits common in TBI.
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Journal of neurotrauma · Aug 2010
High blood glucose does not adversely affect outcome in moderately brain-injured rodents.
In a number of clinical studies researchers have reported that acute hyperglycemia is associated with increased mortality and worsened neurological outcome in patients with traumatic brain injury (TBI). In contrast, it has been demonstrated that intensive insulin therapy to lower blood glucose can lead to an increased frequency of hypoglycemic episodes and poor outcome. Consistent with this, experimental and clinical studies have shown that TBI causes a "metabolic crisis" in the injured brain, suggesting that a reduction in glucose availability may exacerbate brain damage. ⋯ We find that the presence of persistent STZ-induced hyperglycemia results in a reduction of brain edema. Insulin therapy to reduce blood glucose reverses this beneficial effect of hyperglycemia. Taken together, our results indicate that an acute increase in blood glucose levels may not be harmful, and that intervention with insulin therapy to lower blood glucose levels in TBI patients may increase secondary brain damage.