Cervical Collar Clearance in Obtunded Children Presenting Without a Known Traumatic Mechanism: Is Imaging Necessary?

BACKGROUND: Obtunded pediatric patients are often placed in cervical collars (c-collars) to protect their cervical spine (c-spine) while injury is being ruled out, even without a known traumatic injury. The goal of this study was to determine the necessity of c-collars in this population by determining the rate of c-spine injury among patients with suspected non-traumatic mechanisms of loss of consciousness. METHODS: A single institution, ten-year retrospective chart review was conducted including all obtunded patients admitted to the Pediatric Intensive Care Unit without a known traumatic event. Patients were categorized into five groups based on etiology of obtundation: respiratory, cardiac, medical/metabolic, neurologic, and other. Comparisons were made between those placed in a c-collar and a control group who were not, using Wilcoxon rank sum test for continuous measures, and Chi-square or Fisher's exact test for categorical measures. RESULTS: 464 patients were included, of which 39 (8.41%) were placed in a c-collar. There was a significant difference in whether a patient was placed in a c-collar based on diagnosis category (p < 0.001). Those placed in a-c-collar were more likely to undergo imaging studies than the control group (p < 0.001). The overall incidence of c-spine injury in this patient population in our study was zero. CONCLUSION: Cervical collar placement and radiographic evaluation is not necessary in obtunded pediatric patients who present without a known traumatic mechanism as the overall risk of injury is low. Consideration for collar placement should be given in cases when trauma cannot be definitively ruled out at initial evaluation. LEVELS OF EVIDENCE: III.

Regulation of DJ-1 by Glutaredoxin 1 in Vivo: Implications for Parkinson's Disease.

Parkinson's disease (PD) is the second most common neurodegenerative disease worldwide, caused by the degeneration of the dopaminergic neurons in the substantia nigra. Mutations in PARK7 (DJ-1) result in early onset autosomal recessive PD, and oxidative modification of DJ-1 has been reported to regulate the protective activity of DJ-1 in vitro. Glutathionylation is a prevalent redox modification of proteins resulting from the disulfide adduction of the glutathione moiety to a reactive cysteine-SH, and glutathionylation of specific proteins has been implicated in regulation of cell viability. Glutaredoxin 1 (Grx1) is the principal deglutathionylating enzyme within cells, and it has been reported to mediate protection of dopaminergic neurons in Caenorhabditis elegans; however many of the functional downstream targets of Grx1 in vivo remain unknown. Previously, DJ-1 protein content was shown to decrease concomitantly with diminution of Grx1 protein content in cell culture of model neurons (SH-SY5Y and Neuro-2A lines). In the current study we aimed to investigate the regulation of DJ-1 by Grx1 in vivo and characterize its glutathionylation in vitro. Here, with Grx(-/-) mice we provide show that Grx1 regulates protein levels of DJ-1 in vivo. Furthermore, with model neuronal cells (SH-SY5Y) we observed decreased DJ-1 protein content in response to treatment with known glutathionylating agents, and with isolated DJ-1 we identified two distinct sites of glutathionylation. Finally, we found that overexpression of DJ-1 in the dopaminergic neurons partly compensates for the loss of the Grx1 homologue in a C. elegans in vivo model of PD. Therefore, our results reveal a novel redox modification of DJ-1 and suggest a novel regulatory mechanism for DJ-1 content in vivo.