Cortical spreading depression (CSD) is an important disease model for migraine and cerebral ischemia. In this study, we exploit the high temporal and spatial resolution of optical imaging to characterize perfusion-dependent and -independent changes in response to CSD and to investigate the etiology of reflectance changes during CSD. In this experiment, we characterized the optical response to CSD at wavelengths that emphasize perfusion-related changes (610 and 550 nm), and we compared these results with 850 nm and blood volume data. Blood volume changes during CSD were recorded using an intravascular fluorescent dye, Texas Red dextran. We observed triphasic optical signals at 850 and 550 nm characterized by spreading waves of increased, decreased, then increased reflectance (Fig. 1) which expanded at a rate of approximately 3-5 mm/min. The signal at 610 nm had a similar initial phase, but the phase 2 response was slightly more complex, with a parenchymal decrease in reflectance but a vascular increase in reflectance. Reflectance values decreased in phase three. Blood volume signals were delayed relative to the optical intrinsic signals and corresponded temporally to phases 2 and 3. This is the first study to characterize optical imaging of intrinsic signal responses to CSD, in vivo, at multiple wavelengths. The data presented here suggest that changes in light scattering precede perfusion responses, the blood volume increase (phase 2) is accompanied by a reduction in deoxyhemoglobin, and the blood volume decrease (phase 3) is accompanied by an increase in deoxyhemoglobin. Previous studies have suggested the oligemia of spreading depression was a result of decreased metabolic demand. This study suggests that during the oligemic period there is a greater reduction in oxygen delivery than in demand.
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