NeuroImage
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Recovery of function following lesions in the nervous system requires adaptive changes in surviving circuitries. Here we investigate whether changes in cerebral activation are correlated to spinal cord atrophy and recovery of functionality in individuals with incomplete spinal cord injury (SCI). 19 chronic SCI individuals and 7 age-comparable controls underwent functional magnetic resonance imaging (fMRI) while performing rhythmic dorsiflexion of the ankle. A significant negative correlation was found between the activation in the ipsilateral motor (M1) and bilateral premotor cortex (PMC) on one hand and the functional ability of the SCI participants measured by the clinical motor score on the other. ⋯ There was a tendency for a negative correlation between cerebral activation in ipsilateral S1, M1 and PMC and the amplitude of motor evoked potentials in the tibialis anterior muscle elicited by transcranial magnetic stimulation, but this did not reach statistical significance. There was no correlation between motor score or spinal cord dimensions and the volume of the cortical motor areas. The observations show that lesion of descending tracts in the lateral part of the spinal cord results in increased activation in ipsilateral motor and sensory areas, which may help to compensate for the functional deficit following SCI.
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The calibration of functional magnetic resonance imaging (fMRI) for the estimation of neuronal activation-induced changes in cerebral metabolic rate of oxygen (CMRO(2)) has been achieved through hypercapnic-induced iso-metabolic increases in cerebral blood flow (CBF). Hypercapnia (HC) has been traditionally implemented through alterations in the fixed inspired fractional concentrations of carbon dioxide (F(I)CO(2)) without otherwise controlling end-tidal partial pressures of carbon dioxide (P(ET)CO(2)) or oxygen (P(ET)O(2)). There are several shortcomings to the use of this manual HC method that may be improved by using precise targeting of P(ET)CO(2) while maintaining iso-oxia. ⋯ The variability of the calibration constant obtained under HOP (M(HOP)) was 0.3-0.5 that of the HCP one (M(HCP)). In addition, M-variances with precise gas targeting (M(HCP) and M(HOP)) were less than those reported in studies using traditional F(I)CO(2) and F(I)O(2) methods (M(HC) and M(HO), respectively). We conclude that precise controlled gas delivery markedly improves BOLD-calibration for fMRI studies of oxygen metabolism with both the HCP and the more precise HOP-alternative.
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Reliable detection of metabolic changes in the brain in vivo induced by chronic low back pain may provide improved understanding of neurophysiological mechanisms underlying the manifestation of chronic pain. In the present study, absolute concentrations of N-acetyl-aspartate (NAA), creatine (Cr), total choline (tCho), myo-inositol (mI), glutamate (Glu) and glutamine (Gln) were measured in three different pain processing cortical regions (anterior insula, anterior cingulate cortex, and thalamus) of ten patients with non-specific chronic low back pain by means of proton MR spectroscopy ((1)H-MRS) and compared to matched healthy controls. Significant decrease of Glu was observed in the anterior cingulate cortex of patients. ⋯ Reduced concentrations of Glu and Gln may indicate disordered glutamatergic neurotransmission due to prolonged pain perception, whereas decrease of NAA and mI may be ascribed to neuron and glial cell loss. No significant changes were found for Cr. The morphological evaluation of anatomic brain data revealed a significantly decreased WM volume of 17% (p<0.05) as well as a non significant trend for GM volume increase in the anterior insula of patients.
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The effective connectivity networks among overlapped core regions recruited by motor execution (ME) and motor imagery (MI) were explored by means of conditional Granger causality and graph-theoretic method, based on functional magnetic resonance imaging (fMRI) data. Our results demonstrated more circuits of effective connectivity among the selected seed regions during right-hand performance than during left-hand performance, implying the influences of brain asymmetry of right-handedness on effective connectivity networks. ⋯ Furthermore, the In-Out degrees of information flow suggested left dorsal premotor cortex (PMd), inferior parietal lobule (IPL) and superior parietal lobule (SPL) as causal sources in ME/MI tasks, highlighting the dominant function of left PMd, IPL and SPL. These findings depicted the causal connectivity of motor related core regions in fronto-parietal circuit and might indicate the conversion of causal networks between ME and MI.
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This fMRI study was set up to explore how cognitive empathy, i.e. the cognitive inference on another person's affective state, can be characterized as a distinct brain function relating to pre-existing neurofunctional concepts about mentalizing and empathy. In a 3 Tesla MRI scanner 28 healthy participants were presented with four different instructions randomly combined with 32 false-belief cartoon stories of 3 subsequent pictures free of direct cues for affective states, like e.g. facial expressions. Participants were instructed to judge affective or visuospatial changes from their own (1st person perspective) or the protagonists' (3rd person perspective, 3rdpp) perspective. 3rdpp-judgements about affective states differed from visuospatial 3rdpp judgements by a significantly higher activation of the anterior mentalizing network (dorsomedial prefrontal cortex, anterior superior temporal sulcus, temporal poles) and the limbic system (left amygdala and hippocampus). ⋯ The simultaneous activation of the cortical mentalizing network and the amygdala indicates that cognitive empathy actually involves reference to own affective states in the observer. Notably, the cognitive reference to own affective states activated the mentalizing network as well. Moreover our results support pre-existing ideas about a functional anterior-posterior subdivision of the mentalizing network, depending on affective content and 3rd person perspective of cognition.