Journal of neurotrauma
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Journal of neurotrauma · May 2012
Analgesia or addiction?: implications for morphine use after spinal cord injury.
Opioid analgesics are among the most effective agents for treatment of moderate to severe pain. However, the use of morphine after a spinal cord injury (SCI) can potentiate the development of paradoxical pain symptoms, and continuous administration can lead to dependence, tolerance, and addiction. Although some studies suggest that the addictive potential of morphine decreases when it is used to treat neuropathic pain, this has not been studied in a SCI model. ⋯ Exposure to a high concentration of morphine impeded weight gain and locomotor recovery. We suggest that the increased preference observed in injured rats reflects a motivational effect linked in part to the drug's anti-nociceptive effect. Further, although injured rats exhibited a suppression of opiate self-administration, when given access to a high concentration, addictive-like behavior emerged and was associated with poor recovery.
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The current study was undertaken to follow the time course of bone loss in the proximal tibia of rats over several weeks following thoracic contusion spinal cord injury (SCI) of varying severity. It was hypothesized that bone loss would be more pronounced in the more severely injured animals, and that hindlimb weight bearing would help prevent bone loss. Twenty-six female Sprague-Dawley rats (200-225 g, 6-7 weeks old) received standard thoracic (T9) injuries at energies of 6.25, 12.5, 25, or 50 g-cm. ⋯ The 6.25, 12.5 and 25 g-cm groups remained at the same level of bone volume fraction (cancBV/TV=0.24±0.07), while the 50 g-cm group experienced severe bone loss (67%), resulting in significantly lower (p<0.05) bone volume fraction (cancBV/TV=0.11±0.05) at 8 weeks. Proximal tibia cancellous bone strength was reduced by approximately 50% in these severely injured rats. Instead of a linear proportionality between injury severity and bone loss, there appears to be a distinct functional threshold, marked by occasional weight-supported stepping, above which bone loss does not occur.
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Journal of neurotrauma · May 2012
Chronic cervical spinal cord injury: DTI correlates with clinical and electrophysiological measures.
Diffusion tensor imaging (DTI) is rarely applied in spinal cord injury (SCI). The aim of this study was to correlate diffusion properties after SCI with electrophysiological and neurological measures. Nineteen traumatic cervical SCI subjects and 28 age-matched healthy subjects participated in this study. ⋯ The reduced DTI values seen in the SCI subjects are likely due to demyelination and axonal degeneration of spinal tracts, which are related to clinical and electrophysiological measures. A reduction in DTI values in regions remote from the injury site suggests their involvement with wallerian axonal degeneration. DTI can be used for the quantitative evaluation of the extent of spinal cord damage, and eventually to monitor the effects of future regeneration-inducing treatments.
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Journal of neurotrauma · May 2012
The systemic inflammatory response after spinal cord injury in the rat is decreased by α4β1 integrin blockade.
Abstract The systemic inflammatory response syndrome (SIRS) follows spinal cord injury (SCI) and causes damage to the lungs, kidney, and liver due to an influx of inflammatory cells from the circulation. After SCI in rats, the SIRS develops within 12 h and is sustained for at least 3 days. We have previously shown that blockade of CD11d/CD18 integrin reduces inflammation-driven secondary damage to the spinal cord. ⋯ Treatment effects were less robust in the kidney. Overall, the efficacy of the anti-α4β1 treatment did not differ greatly from that of the anti-CD11d antibody, although details of the results differed. The SIRS after SCI impedes recovery, and attenuation of the SIRS with an anti-integrin treatment is an important, clinically-relevant finding.
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Journal of neurotrauma · May 2012
Cauda equina repair in the rat: part 2. Time course of ventral root conduction failure.
Treatment for cauda equina (CE) ventral root injury is currently limited. Furthermore, relatively little is known about the time course of nerve root functional degeneration after such injury has occurred. Using a previously developed method for identifying spinal nerve roots that innervate the rat tail, we transected S2, S3, and S4 ventral roots and measured their ability to activate tail muscles out to 72 h post-injury by way of stimulus-evoked electromyography (EMG) recording. ⋯ This percentage dropped to 39% at 48 h, and just 18% at 72 h. Moving 5 mm from the site of injury, we identified 83% intact axons at 24 h post-transection, 77% at 48 h, and 68% at 72 h. Regenerative implications aside, if electrophysiological mapping of injured nerve roots is to be carried out for repair purposes, the rapid nature of conduction failure needs to be considered.