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  • Presented at the 2013 AAPM Annual Meeting « Back

    107

    Sensitization of the Human Spinal Cord in the Absence Of Pain

    Brittney R. Reyes, BA, reyes89@stanford.edu1, Paul G. Nash, PhD1, Emily K. Hubbard, BA2, Sean Mackey, MD PhD1, (1) Stanford University, Palo Alto, California, (2) Stanford University School of Medicine, San Francisco, California

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    Introduction: Central sensitization is a major contributing factor to the maintenance of a number of chronic pain conditions. While the spinal mechanisms are thought to contribute to symptoms described by patients, such as allodynia and hyperalgesia, they are yet to be shown in humans. The aims of this study were to image central sensitization in the human spinal cord using resting state functional MRI. This study used two experimental groups, sensitized and non-sensitized. Subjects were sensitized using the heat capsaicin model (Petersen and Rowbotham, 1999). Non-sensitized subjects had no capsaicin applied. Following the establishment of the model on the volar forearm, we collected two fMRI scans: 1. A heat pain scan, which we used to functionally define the dorsal horn. 2. Resting state scan. Images were preprocessed using SPM8. Changes in signal intensity in the heat pain scans were determined using a box-car model convolved with a hemodynamic response function. We used the most significant cluster in the dorsal horn from the heat pain analysis as a region of interest to extract the time courses from the resting state data. The time courses were used as regressors in individual analyses. Individual connectivity maps were then combined to give group connectivity maps. The primary findings of this study were an increased functional connectivity in the spinal cord of sensitized subjects with no pain compared to non-sensitized subjects. This study provides evidence of central sensitization at the level of the spinal cord in the absence of perceived of pain. References: 1) Petersen KL, Rowbotham MC. A new human experimental pain model: the heat/capsaicin sensitization model. Neuroreport 10:1511-1516.1999.

    Funding: This study was supported by NIH funds: R01 NS053961

    Poster 107

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