Journal of neurotrauma
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Journal of neurotrauma · Jul 2011
Cortical excitability changes in patients with sleep-wake disturbances after traumatic brain injury.
Although chronic sleepiness is common after head trauma, the cause remains unclear. Transcranial magnetic stimulation (TMS) represents a useful complementary approach in the study of sleep pathophysiology. We aimed to determine in this study whether post-traumatic sleep-wake disturbances (SWD) are associated with changes in excitability of the cerebral cortex. ⋯ Similarly to that reported in patients with narcolepsy, the cortical hypoexcitability may reflect the deficiency of the excitatory hypocretin/orexin-neurotransmitter system. These observations may provide new insights into the causes of chronic sleepiness in patients with TBI. A better understanding of the pathophysiology of post-traumatic SWD may also lead to better therapeutic strategies in these patients.
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Journal of neurotrauma · Jul 2011
Comparative StudyObjective measures of motor dysfunction after compression spinal cord injury in adult rats: correlations with locomotor rating scores.
Precise assessment of motor deficits after traumatic spinal cord injury (SCI) in rodents is crucial for understanding the mechanisms of functional recovery and testing therapeutic approaches. Here we analyzed the applicability to a rat SCI model of an objective approach, the single-frame motion analysis, created and used for functional analysis in mice. Adult female Wistar rats were subjected to graded compression of the spinal cord. ⋯ FSA co-varied with RHI only in the severely impaired rats, while RHI and CLS were barely correlated. Our findings suggest that the numerical parameters estimate, as intended by design, predominantly different aspects of locomotion. The use of these objective measures combined with BBB rating provides a time- and cost-efficient opportunity for versatile and reliable functional evaluations in both severely and moderately impaired rats, combining clinical assessment with precise numerical measures.
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Journal of neurotrauma · Jul 2011
The combination of either tempol or FK506 with delayed hypothermia: implications for traumatically induced microvascular and axonal protection.
Following traumatic brain injury (TBI), inhibition of reactive oxygen species and/or calcineurin can exert axonal and vascular protection. This protection proves optimal when these strategies are used early post-injury. Recent work has shown that the combination of delayed drug administration and delayed hypothermia extends this protection. ⋯ These studies illustrate the potential benefits of Tempol coupled to delayed hypothermia. However, these findings do not transfer to the use of FK506, which in previous studies proved beneficial when coupled with hypothermia. These divergent results may be a reflection of the different animal models used and/or their associated injury severity.
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Journal of neurotrauma · Jul 2011
Predictive and associated factors of psychiatric disorders after traumatic brain injury: a prospective study.
Psychiatric disorders are common and often debilitating following traumatic brain injury (TBI). However, there is little consensus within the literature regarding the risk factors for post-injury psychiatric disorders. A 1-year prospective study was conducted to examine which pre-injury, injury-related, and concurrent factors were associated with experiencing a psychiatric disorder, diagnosed using the Structured Clinical Interview for DSM-IV-TR Axis I Disorders, at 1 year post-injury. ⋯ Limb injury also emerged as a useful early indicator of later psychiatric disorder. Post-injury psychiatric disorders were associated with concurrent unemployment, pain, poor quality of life, and use of unproductive coping skills. The clinical implications of these findings are discussed.
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Journal of neurotrauma · Jul 2011
Glycomimetic improves recovery after femoral injury in a non-human primate.
In adult mammals, restoration of function after peripheral nerve injury is often poor and effective therapies are not available. Previously we have shown in mice that a peptide which functionally mimics the human natural killer cell (HNK)-1 trisaccharide epitope significantly improves the outcome of femoral nerve injury. Here we evaluated the translational potential of this treatment using primates. ⋯ Better outcome at 160 days after surgery in treated versus control animals was also confirmed by improved quadriceps muscle force, enhanced H-reflex amplitude, decreased H-reflex latency, and larger diameters of regenerated axons. No adverse reactions to the mimetic, in particular immune responses resulting in antibodies against the HNK-1 mimetic or immune cell infiltration into the damaged nerve, were observed. These results indicate the potential of the HNK-1 mimetic as an efficient, feasible, and safe adjunct treatment for nerve injuries requiring surgical repair in clinical settings.