An open-source automated platform for three-dimensional visualization of subdural electrodes using CT-MRI coregistration.

OBJECTIVE: Visualizing implanted subdural electrodes in three-dimensional (3D) space can greatly aid in planning, executing, and validating resection in epilepsy surgery. Coregistration software is available, but cost, complexity, insufficient accuracy, or validation limit adoption. We present a fully automated open-source application, based on a novel method using postimplant computerized tomography (CT) and postimplant magnetic resonance (MR) images, for accurately visualizing intracranial electrodes in 3D space. METHODS: CT-MR rigid brain coregistration, MR nonrigid registration, and prior-based segmentation were carried out on seven patients. Postimplant CT, postimplant MR, and an external labeled atlas were then aligned in the same space. The coregistration algorithm was validated by manually marking identical anatomic landmarks on the postimplant CT and postimplant MR images. Following coregistration, distances between the center of the landmark masks on the postimplant MR and the coregistered CT images were calculated for all subjects. Algorithms were implemented in open-source software and translated into a "drag and drop" desktop application for Apple Mac OS X. RESULTS: Despite postoperative brain deformation, the method was able to automatically align intrasubject multimodal images and segment cortical subregions, so that all electrodes could be visualized on the parcellated brain. Manual marking of anatomic landmarks validated the coregistration algorithm with a mean misalignment distance of 2.87 mm (standard deviation 0.58 mm)between the landmarks. Software was easily used by operators without prior image processing experience. SIGNIFICANCE: We demonstrate an easy to use, novel platform for accurately visualizing subdural electrodes in 3D space on a parcellated brain. We rigorously validated this method using quantitative measures. The method is unique because it involves no preprocessing, is fully automated, and freely available worldwide. A desktop application, as well as the source code, are both available for download on the International Epilepsy Electrophysiology Portal (https://www.ieeg.org) for use and interactive refinement.

Controlled cortical impact traumatic brain injury acutely disrupts wakefulness and extracellular orexin dynamics as determined by intracerebral microdialysis in mice.

Among other deficits, traumatic brain injury (TBI) causes impaired arousal and cognitive dysfunction. Hypothalamic orexin neuropeptides (also called hypocretins) regulate levels of arousal, and cerebrospinal fluid orexin levels are reportedly low in TBI patients. We hypothesized that TBI acutely impairs the dynamics of orexin release into brain interstitial fluid, and that these extracellular orexin levels correlate with wakefulness and motor activity. To test this in mice, we combined an electromagnetic controlled cortical impact (CCI) model of experimental TBI with dual intracerebral microdialysis using one catheter in the hypothalamus and one catheter in the hippocampus, plus electroencephalography/electromyography (EEG/EMG), and motor activity monitoring. Baseline data were continuously collected in tethered but relatively freely moving mice for 2 days. Then, ipsilateral CCI or sham surgery was performed, and data collection was continued for 3 additional days. At baseline, extracellular orexin levels in the hypothalamus showed a circadian rhythm, with peak levels during the dark (wake) phase, and a nadir during the light (rest) phase. Following CCI but not sham surgery, orexin levels were depressed in both the hypothalamus and hippocampus, and diurnal fluctuation amplitudes were blunted in the hypothalamus. At baseline, correlations of orexin with wakefulness and motor activity were positive and highly significant. Following CCI but not sham surgery, the mice exhibited reduced wakefulness and motor activity, and correlations between orexin and these measures were diminished. These abnormal orexin dynamics were associated with hypothalamic astrogliosis, but not acute loss of orexin neurons, as assessed by immunohistochemistry 3 days after injury. Future studies involving experimental manipulations of the orexin system will be required to determine its contribution to neurological outcomes following injury.