Journal of neurotrauma
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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.
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Amiloride is a drug approved by the United States Food and Drug Administration, which has shown neuroprotective effects in different neuropathological conditions, including brain injury or brain ischemia, but has not been tested in spinal cord injury (SCI). We tested amiloride's therapeutic potential in a clinically relevant rat model of contusion SCI inflicted at the thoracic segment T10. ⋯ Our data indicate that higher levels of MOG correlate with improved locomotor recovery after SCI, and that this may explain the beneficial effects of amiloride after SCI. Given that amiloride treatment after SCI caused a significant preservation of myelin levels, and improved locomotor recovery, it should be considered as a possible therapeutic intervention after SCI.
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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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Visual pursuit is a key descriptor of the minimally conscious state (above 80% of cases). It is also observable in about 20% of subjects in vegetative state. Its reappearance after severe brain damage anticipates a favorable outcome, with recovery of consciousness in 73% of subjects (45% in the absence of it). ⋯ After 230 days of follow-up or more, it was observed in 89% and 88% of post-traumatic and vascular subjects and in 67% of anoxic-hypoxic patients. Rating with the Glasgow Outcome Scale (GOS) was better in those subjects with recovered visual tracking and inversely correlated with the time of reappearance in post-traumatic and vascular subjects; also the subjects with late recovery of eye tracking (230 days or more) had better GOS outcome than those without it. The observation of visual tracking reappearing in subjects in vegetative state would reflect recuperation of the brainstem-cortical interaction and overall brain functional organization that are thought to sustain consciousness and are interfered with by the "functional disconnection," resulting in the vegetative state.
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Journal of neurotrauma · Jul 2011
Short-term moderate hypocapnia augments detection of optimal cerebral perfusion pressure.
An autoregulation-oriented strategy has been proposed to guide neurocritical therapy toward the optimal cerebral perfusion pressure (CPPOPT). The influence of ventilation changes is, however, unclear. We sought to find out whether short-term moderate hypocapnia (HC) shifts the CPPOPT or affects its detection. ⋯ Moderate HC did not shift this CPPOPT but enabled its detection in another 17 patients (CPPOPT left: 83.94±14.82; right: 85.28±14.73 mm Hg). The detection of CPPOPT was achieved via significantly improved Mx-autoregulatory index and an increase of CPP mean. It appeared that short-term moderate HC augmented the detection of an optimum CPP, and may therefore usefully support CPP-guided therapy in patients with TBI.