NeuroImage
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According to meta-analyses, depression is associated with a smaller hippocampus. Most magnetic resonance imaging (MRI) studies among middle aged acute depressed patients are based on manual segmentation of the hippocampus. Few studies used automated methods such as voxel-based morphometry (VBM) or automated segmentation that can overcome certain drawbacks of manual segmentation (essentially intra- and inter-rater variability and operator time consumption). ⋯ Using VBM-DARTEL, when corrected for multiple comparisons, significant volume differences were detected between groups in different regions and more specifically in hippocampus with ROI analyses. Whereas using standard VBM (without DARTEL), ROI analyses did not show bilateral volume between group differences. Significant hippocampal volume reductions between patients and controls were also detected using manual segmentation (-11.6% volume reduction, p<0.05) and automated segmentation (-9.7% volume reduction, p<0.05). VBM-DARTEL and automated segmentation show equal sensitivity in detecting hippocampal differences in depressed patients, while standard VBM was unable to detect hippocampal changes. Both VBM-DARTEL and automated segmentation could be used to perform large scale volumetric studies in humans. The new automated segmentation technique could further explore and detect hippocampal subpart differences that could be very useful for clarifying physiopathology of psychiatric disorders.
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Distinct aspects of our fearful experiences appear to be mediated by separate explicit and implicit memory processes. To identify brain regions that support these separate memory processes, we measured contingency awareness, conditional fear expression, and functional magnetic resonance imaging signal during a Pavlovian fear conditioning procedure in which tones that predicted an aversive event were presented at supra and sub-threshold volumes. ⋯ In contrast, conditional fear and differential amygdala activity developed on both perceived and unperceived trials, regardless of whether contingency awareness was expressed. These findings demonstrate the distinct roles of these brain regions in explicit and implicit fear memory processes.
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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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Previous studies have established regional gray matter (GM) volume loss in multiple sclerosis (MS) but the relationship between development of white matter (WM) lesions and changes of regional GM volumes is unclear. The present study addresses this issue by means of voxel-based morphometry (VBM). T1-weighted three-dimensional magnetic resonance imaging (MRI) data from MS patients followed up for 12 months were analyzed using VBM. ⋯ Within the RRMS group, those patients with increasing T2 and T1 lesion burden (n=45) showed additional GM volume loss during follow-up in the frontal and parietal cortex, and precuneus. In contrast, patients lacking an increase in WM lesion burden (n=44) did not show any significant GM changes. The present study suggests that the progression of regional GM volume reductions is associated with WM lesion progression and occurs predominantly in fronto-temporal cortical areas.
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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.