Journal of neurotrauma
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Journal of neurotrauma · May 2012
Maximum principal strain correlates with spinal cord tissue damage in contusion and dislocation injuries in the rat cervical spine.
The heterogeneity of the primary mechanical mechanism of spinal cord injury (SCI) is not currently used to tailor treatment strategies because the effects of these distinct patterns of acute mechanical damage on long-term neuropathology have not been fully investigated. A computational model of SCI enables the dynamic analysis of mechanical forces and deformations within the spinal cord tissue that would otherwise not be visible from histological tissue sections. We created a dynamic, three-dimensional finite element (FE) model of the rat cervical spine and simulated contusion and dislocation SCI mechanisms. ⋯ Average peak principal strains were compared to tissue damage measured previously in the same regions via axonal permeability to 10-kD fluorescein-dextran. Linear regression of tissue damage against peak maximum principal strain for pooled data within all white matter regions yielded similar and significant (p<0.0001) correlations for both contusion (R(2)=0.86) and dislocation (R(2)=0.52). The model enhances our understanding of the differences in injury patterns between SCI mechanisms, and provides further evidence for the link between principal strain and tissue damage.
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Traumatic neuroma in continuity (NIC) results in profound neurological deficits, and its management poses the most challenging problem to peripheral nerve surgeons today. The absence of a clinically relevant experimental model continues to handicap our ability to investigate ways of better diagnosis and treatment for these disabling injuries. Various injury techniques were tested on Lewis rat sciatic nerves. ⋯ We have demonstrated histological features and poor functional recovery consistent with NIC formation in a rat model. The injury mechanism employed combines traction and compression forces akin to the physical forces at play in clinical nerve injuries. This model may serve as a tool to help diagnose this injury earlier and to develop intervention strategies to improve patient outcomes.
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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
Re-innervation of the bladder through end-to-side neurorrhaphy of autonomic nerve and somatic nerve in rats.
End-to-side neurorrhaphy is widely used in the peripheral nervous system for nerve repair; however, the application of this technique has been limited to somatic nerves. The feasibility of nerve regeneration through end-to-side neurorrhaphy between autonomic and somatic nerves with different characteristics in the peripheral nervous system is still undetermined. In this study, rats were divided into three groups for different treatments (n=10 per group). ⋯ Morphological examination and intravesical pressure measurement indicated prominent nerve regeneration and successful re-innervation of the bladder in the neurorrhaphy group, compared with the "no repair" group (p<0.05). No significant changes were observed in the histology of the donor nerve and the bilateral extensor digitorum longus muscles in the neurorrhaphy group. Nerve regeneration may be achievable for nerve repair through end-to-side neurorrhaphy between autonomic and somatic nerves without apparent impairment of donor somatic nerve.
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Journal of neurotrauma · May 2012
Transplantation of mesenchymal stem cells promotes an alternative pathway of macrophage activation and functional recovery after spinal cord injury.
Mesenchymal stem cells (MSC) derived from bone marrow can potentially reduce the acute inflammatory response in spinal cord injury (SCI) and thus promote functional recovery. However, the precise mechanisms through which transplanted MSC attenuate inflammation after SCI are still unclear. The present study was designed to investigate the effects of MSC transplantation with a special focus on their effect on macrophage activation after SCI. ⋯ This was associated simultaneously with increased numbers of alternatively activated macrophages (M2 phenotype: arginase-1- or CD206-positive), and decreased numbers of classically activated macrophages (M1 phenotype: iNOS- or CD16/32-positive). These changes were associated with functional locomotion recovery in the MSC-transplanted group, which correlated with preserved axons, less scar tissue formation, and increased myelin sparing. Our results suggested that acute transplantation of MSC after SCI modified the inflammatory environment by shifting the macrophage phenotype from M1 to M2, and that this may reduce the effects of the inhibitory scar tissue in the subacute/chronic phase after injury to provide a permissive environment for axonal extension and functional recovery.