Journal of neurotrauma
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Journal of neurotrauma · Dec 2012
Degeneration of phrenic motor neurons induces long-term diaphragm deficits following mid-cervical spinal contusion in mice.
A primary cause of morbidity and mortality following cervical spinal cord injury (SCI) is respiratory compromise, regardless of the level of trauma. In particular, SCI at mid-cervical regions targets degeneration of both descending bulbospinal respiratory axons and cell bodies of phrenic motor neurons, resulting in deficits in the function of the diaphragm, the primary muscle of inspiration. Contusion-type trauma to the cervical spinal cord is one of the most common forms of human SCI; however, few studies have evaluated mid-cervical contusion in animal models or characterized consequent histopathological and functional effects of degeneration of phrenic motor neuron-diaphragm circuitry. ⋯ We report that phrenic motor neuron loss in cervical spinal cord, phrenic nerve axonal degeneration, and denervation at diaphragm neuromuscular junctions (NMJ) resulted in compromised ipsilateral diaphragm function, as demonstrated by persistent reduction in diaphragm compound muscle action potential amplitudes following phrenic nerve stimulation and abnormalities in spontaneous diaphragm electromyography (EMG) recordings. This injury paradigm is reproducible, does not require ventilatory assistance, and provides proof-of-principle that generation of unilateral cervical contusion is a feasible strategy for modeling diaphragmatic/respiratory deficits in mice. This study and its accompanying analyses pave the way for using transgenic mouse technology to explore the function of specific genes in the pathophysiology of phrenic motor neuron degeneration and respiratory dysfunction following cervical SCI.
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Journal of neurotrauma · Dec 2012
The frontal lobe and thalamus have different sensitivities to hypoxia-hypotension after traumatic brain injury: a microdialysis study in rats.
After traumatic brain injury (TBI), lesions are anatomically heterogeneous, but the spatial heterogeneity of the post-traumatic brain's vulnerability to hypoxia-hypotension (HH) has been poorly studied. Our objective was to compare the effect of HH after TBI on brain energy metabolism into two regions: the frontal lobe and the thalamus. Twenty-eight Sprague-Dawley rats were randomized into four groups: sham, TBI (brain trauma alone, impact acceleration, 450-g weight drop from 1.8 m), HH (blood depletion to mean arterial pressure 40 mm Hg, FiO(2) 10%, 15 min), and TBI-HH (TBI followed by HH, 45-min delay). ⋯ During the 30 min following the HH phase (reperfusion), an increase in PtiO(2) was observed. In the TBI-HH group, this increase was significantly lower in the frontal lobe than in the thalamus. These findings demonstrate that in the early post-traumatic period, the metabolic cerebral response to HH is higher in the frontal lobe than in the thalamus, and is worsened by TBI, suggesting a higher vulnerability for the frontal lobes.
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Journal of neurotrauma · Dec 2012
Does timing of surgery affect hospitalization costs and length of stay for acute care following a traumatic spinal cord injury?
Although there is a trend toward performing early surgery for traumatic spinal cord injury (SCI), it remains unclear whether this tendency leads to decreased costs and length of stay (LOS) for acute care. This study determined the impact of surgical timing on costs and LOS after a traumatic SCI. A total of 477 consecutive patients sustaining an acute traumatic SCI and receiving surgery at a level I trauma center were included. ⋯ LOS was associated with the surgical delay dichotomized into two groups (<24 vs. ≥24 h), as well as with age, ISS, ASIA grade, and neurological level. This study suggests that resource utilization in terms of costs and LOS for the acute hospitalization is decreased with early surgery after an acute traumatic SCI, particularly if the procedure is performed within 24 h following the trauma. Performing the surgery as early as possible when the patient is cleared for surgery could lower the financial burden on the healthcare system, while optimizing the neurological recovery.
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Journal of neurotrauma · Dec 2012
Expectations of benefit and tolerance to risk of individuals with spinal cord injury regarding potential participation in clinical trials.
We conducted a survey of individuals living with spinal cord injury (SCI) to determine their receptivity to participating in clinical trials of drug therapies or stem cell therapies, their anticipation of therapeutic benefits, and their tolerance to risk. A 46-item questionnaire was administered to individuals with cervical or thoracic SCI identified through a provincial database. The average age was 42 years and the individuals were, on average, 5.5 years post-injury. ⋯ Injury severity or chronicity did not have a significant correlation with risk tolerance. Whereas previous studies have shown that the understanding of stem cell science is limited among individuals with SCI, here we show that many still have high hopes for the possibility of neurological benefit, are anxious to participate in invasive stem cell trials, and, in many cases, have high tolerance for risk in such trials. Taken together, the data underscore the need for careful communication with individuals with SCI to avoid unrealistic expectations and therapeutic misconception in experimental trials.
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Journal of neurotrauma · Dec 2012
The expression of α-SMA in the painful traumatic neuroma: potential role in the pathobiology of neuropathic pain.
The exact mechanism of neuroma-associated pain is not yet fully understood, thus contributing to the substantial challenge faced in managing patients with painful neuromas. We aimed to observe the expression of alpha smooth muscle actin (α-SMA) in the painful traumatic neuroma and to investigate its possible roles in the cause of neuroma-associated pain. Its expression is considered to be a useful phenotypic marker for myofibroblast, and may contribute to its increased contractile activity. ⋯ Linear regression analysis indicated that the expression intensity of α-SMA was positively related to the scale of VAS (R(2)=0.691, p<0.001). These findings suggest that: 1) expression of α-SMA may play certain roles in painful traumatic neuroma, either as a direct cause of neuroma-associated pain or as an indirect marker of local mechanical stimuli, and 2) the presence of α-SMA in the painful group may provide rationale for transpositional procedures in the management of traumatic neuroma. The persistent existence of α-SMA in the painful group and the correlation with VAS scores may provide insight into the development of new therapeutic strategies.