NeuroImage
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Cortical spreading depression (i.e. waves of cellular depolarization, CSD) causes the aura symptoms in classical migraine, and may contribute to delayed cellular damage after an ischemic or traumatic insult to the brain. In the latter cases, secondary neuronal injury may be worsened by some of the cerebral blood flow (CBF) changes that are associated with CSD. Here, we describe a new method for the simultaneous, live imaging of local cellular depolarization and CBF changes (i.e. two variables with well-defined and important biological significance), through a closed cranial window prepared in anesthetized rats. ⋯ In addition to the high temporal and spatial resolution of VS dye and LSC imaging, their novel combination allows to determine how CBF changes relate to a heterogeneous and evolving pattern of cellular depolarization, in any area of interest of the cortical region under study. This methodological development is especially pertinent and timely for investigations into the peri-lesion depolarizations that occur in models of focal brain injury, situations where their site of spontaneous elicitation and propagation pattern cannot be predicted. It should also help advance our knowledge in epilepsy, CBF pharmacology, and neurovascular coupling under normal and pathophysiological conditions.
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Pain is associated with the activation of many brain areas involved in the multiple dimensions of the experience. Several of those brain areas may also contribute to the monitoring and regulation of autonomic activity but this aspect of pain responses has been largely overlooked in human imaging studies. This functional magnetic resonance imaging (fMRI) study relied on blood-oxygen level dependent (BOLD) signal to investigate subject-related differences in brain activity associated with the individual differences in electrodermal responses evoked by 30 s noxious (pain) and innocuous (warm) thermal stimuli. ⋯ Subjects showing larger skin conductance reactivity to the innocuous and/or noxious stimuli displayed larger stimulus-evoked brain responses in the somato-motor cortices (SI/MI, SII, and insula), the perigenual and supracallosal ACC, the orbitofrontal cortex and the medulla. Further analyses revealed brain activation more specifically associated with the pain-related skin conductance reactivity in the supracallosal ACC, amygdala, thalamus, and hypothalamus. These findings demonstrate that individual differences in electrodermal reactivity partly reflect differences in pain-evoked brain responses, consistent with a role of these structures in the monitoring/regulation of pain-related autonomic processes.
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The blood-oxygenation-level-dependent (BOLD) signal is dependent on multiple physiological factors such as cerebral blood flow (CBF), local oxygen metabolism (CMRO(2)) and cerebral blood volume (CBV). Since caffeine affects both CBF and neural activity, its effects on BOLD remain controversial. The calibrated BOLD approach is an excellent tool to study caffeine because it combines CBF and BOLD measures to estimate changes in CMRO(2). ⋯ The results show that caffeine decreases n, the CBF:CMRO(2) coupling ratio, from 2.58 to 2.33 in motor (p=0.006) and from 2.45 to 2.23 in visual (p=0.002) areas respectively. The current study also demonstrated that caffeine does not alter cerebrovascular reactivity to CO(2). These results highlight the importance of the calibrated BOLD approach in improving interpretation of the BOLD signal in the presence of substances like caffeine.
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The changes of directional diffusivities derived from diffusion tensor imaging (DTI), i.e. decreased axial diffusivity (lambda(||)) and increased radial diffusivity (lambda( perpendicular)), have shown significant correlation with axonal and myelin damage, respectively. However, after formalin fixation, reduced sensitivity of lambda(||) in detecting axonal damage in tissue has raised the concern of applying DTI ex vivo. In order to distinguish whether death or the fixation process diminishes the sensitivity of DTI in detecting lesions, in vivo, pre-fixed postmortem, and fixed postmortem DTI were conducted on mouse optic nerves 3 and 14 days after transient retinal ischemia. ⋯ From pre-fixed postmortem to fixed postmortem, lambda(||) and lambda( perpendicular) decreased by 40 to 50% in normal and 3-day injured optic nerves, but only by 15 to 25% in 14-day injured optic nerves. Consequently, for the 14-day injured optic nerves, the differences between healthy and injured nerves were not preserved after fixation: the 40% decreased lambda(||) and 200% increased lambda( perpendicular) in injured nerves as compared to the normal nerves were measured in vivo and pre-fixed postmortem, but after the fixation process, 300% increased lambda( perpendicular) and insignificant changes in lambda(||) were found in injured nerves as compared to the normal nerves. This study clarified that fixation process, but not death, could change the sensitivity of DTI in detecting injury.
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Comparative Study
Sensitivity of voxel-based morphometry analysis to choice of imaging protocol at 3 T.
The objective of this study was to determine which 3D T(1)-weighted acquisition protocol at 3 T is best suited to voxel-based morphometry (VBM), and to characterize the sensitivity of VBM to choice of acquisition. First, image quality of three commonly used protocols, FLASH, MP-RAGE and MDEFT, was evaluated in terms of SNR, CNR, image uniformity and point spread function. These image metrics were estimated from simulations, phantom imaging and human studies. ⋯ The required population sample size estimates to detect a difference in GM density in longitudinal VBM studies, i.e. based only on methodological variance, were lowest for MDEFT. Although MP-RAGE requires more subjects than FLASH, its higher cortical CNR improves the accuracy of the tissue classification results, particularly in the motor cortex. For cross-sectional VBM studies, the variance in morphology across the population is likely to be the primary source of variability in the power analysis.