Postinjury inflammation has been implicated in secondary degeneration following injury to the spinal cord. The cellular inflammatory response to injury has not been described in the lateral compression injury model, although various types of compression injuries account for 20% of human spinal cord injuries (SCI). Here, we used forceps to induce a moderate compression injury to the thoracic spinal cord of female Sprague-Dawley rats. We evaluated innate and adaptive components of the inflammatory response at various times postinjury using immunohistochemical techniques. We show that components of innate immunity (e.g., macrophages and dendritic cells) peak between 1 and 2 weeks postinjury but persist through 42 days postinjury (dpi). CD163 and CD206 expression, associated with an anti-inflammatory, reparative phenotype, was upregulated on activated macrophages in the injury site, as were MHC class II antigens. The expression of MHC class II antigens is necessary for the initiation of adaptive immunity and was accompanied by an influx of T cells. T cells were initially restricted to gray matter at the injury epicenter but were later observed throughout the lesioned parenchyma. In summary, we demonstrate that lateral forceps compression of the spinal cord produces a neuroinflammatory response similar to that described in human spinal cord trauma and in other experimental models of spinal cord trauma, thus is an appropriate model to study secondary neurodegeneration in SCI.

This prospective case series compared the accuracy of ultrasound (US) to magnetic resonance imaging (MRI) in differentiating complete displaced (CD) thumb ulnar collateral ligament (UCL) tears from nondisplaced injuries in 10 patients with suspected traumatic thumb UCL injuries. Ultrasound identified 100% (2 of 2) of MRI‐documented CD tears, both of which were further confirmed during surgical repair. Ultrasound identified the absence of CD tears in the remaining 8 patients. Although MRI is the reference standard imaging modality for characterizing thumb UCL injuries, ultrasound should be considered an accurate, cost‐effective, and alternative imaging modality to differentiate surgical versus nonsurgical thumb UCL injuries.

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We sought to evaluate the neuroinflammatory response in a compression model of spinal cord injury (SCI). Because compression is a common mechanism of injury in human spinal cord trauma, such a model has clinical relevance. In this study we used forceps to induce lateral compression injury to the spinal cord, producing a moderate degree of injury as previously described in the contusion model (Basso et al., 1996).Post‐injury inflammation has been implicated in secondary degeneration but has not been characterized in this model. We evaluated the inflammatory response in the injured spinal cord using immunohistochemistry. We found that neutrophils are present within the lesion site by 1 day post injury (dpi) but do not persist past 3 dpi. T‐cells were present by 1 dpi, mainly in gray matter at the epicenter. They peaked in number at 7 dpi, but persisted to 42 dpi. A similar time course was observed for macrophage activation, although the response was more widespread at the impact site and extended further rostrocaudally. Overall, we confirm that forceps compression of the spinal cord produces a neuroinflammatory response similar to what has been described in human spinal cord trauma and in contusion models of experimental spinal cord trauma. Thus, forceps compression represents a clinically relevant experimental model for evaluating secondary injury.Grant Funding Source: MWU Biomedical Sciences program

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