Dynamic Detection of Spinal Cord Position During Postural Changes Using Near-Infrared Reflectometry.

INTRODUCTION: Motion of the spinal cord relative to a spinal cord stimulator epidural electrode array can cause suboptimal stimulation: either noxious, inefficient, or insufficient. Adaptive stimulation attempts to mitigate these effects by modulating stimulation parameters in a position-dependent fashion. Near-infrared (NIR) reflectometry is demonstrated to provide real-time direct measurement of spinal cord position at the site of stimulation, which can facilitate closed-loop adaptive stimulation during static and dynamic motion states. METHODS: A miniature sensor array consisting of an NIR light emitting diode flanked by phototransistors potted in epoxy was placed in the dorsal epidural space of a human cadaver at the T8 level via laminotomy. Turgor of the subarachnoid space was maintained by intrathecal infusion of saline. NIR reflectance was measured as the cadaver was rotated about its longitudinal axis on a gantry. NIR reflectance was correlated with gantry position and velocity. RESULTS: NIR reflectometry suggests gravitational force is the primary determinant of cord position in static, ordinal positions. Under dynamic motion conditions, there was statistically significant cross-correlation between reflectometry data and the tangential velocity squared, suggesting that centripetal force was the primary determinant of cord position as the gantry was rotated. Reflectometry data strongly correlated with a simple geometric model of anticipated spinal cord precession within the spinal canal. CONCLUSIONS: Spinal cord position during dynamic motion has been shown to differ from static predictions due to additional influences such as centripetal force. These findings underscore limitations in extrapolating spinal cord position from surrogates such as body position or body acceleration at sites remote from the stimulating electrodes. NIR reflectometry offers a real-time direct measure of spinal cord position in both static and dynamic motion states, which may facilitate closed-loop adaptive stimulation applications.

Role of basic fibroblast growth factor in the course of cerebral vasospasm in an experimental model of subarachnoid hemorrhage.

The goal of this study was to investigate the relationship between basic fibroblast growth factor (bFGF) and the course of cerebral vasospasm after subarachnoid hemorrhage (SAH), using an immunohistochemical method. Female Sprague-Dawley rats were sacrificed by perfusion fixation 10 min, 6 h, 1, 2, 3, 4, 7 or 14 days after a single intracisternal injection of fresh autologous arterial blood. Morphometric analysis of lumen cross-sectional areas of blood vessels were determined by computerized image analysis. Results were expressed as percent lumen patency, defined as the ratio of the area of vessel patency in SAH rats to the area of patency in control rats. An immunohistochemical analysis against bFGF was performed using the avidin-biotin-peroxidase technique. The immuno-reactivity of bFGF was observed with the aid of a light microscope and semiquantitatively graded. Basilar arterial spasm was greatest 10 min after SAH (mean decrease: 67.1% of the control values; p < 0.001). Subsequently, there was a significant degree of spasm of the artery for three days after SAH, followed by full recovery at day 4. A slight increase in immunoreactivity was observed in the intima only at 10 min and one day after SAH. In the media, immunoreactivity showed a biphasic pattern; a significant increase in immunoreactivity was observed at 10 min that persisted for two days after SAH. At three days after SAH, immunoreactivity in the media returned to the control level, but then gradually increased significantly to reach a maximum at 14 days after SAH while the vascular dimensions were normal. Immunohistochemical analysis failed to show a direct relationship between bFGF and the course of cerebral vasospasm in this rat single-hemorrhage model. However, the late phase upregulation of bFGF might lead to the vascular angiopathy, fibrosis or hyperplasia during the chronic stage of SAH.