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Objective. Previous work suggests that the perception of pain is subjective and dependent on individual differences in physiological, emotional, and cognitive states. Functional magnetic resonance imaging (FMRI) studies have used both stimulusrelated (nociceptive properties) and percept-related (subjective experience of pain) models to identify the brain networks associated with pain. Our objective was to identify the network involved in processing subjective pain during cold stimuli. Methods. The current FMRI study directly contrasted a stimulus-related model with a perceptrelated model during blocks of cold pain stimuli in healthy adults. Specifically, neuronal activation was modelled as a function of changes in stimulus intensity vs as a function of increasing/decreasing levels of subjective pain corresponding to changes in pain ratings. In addition, functional connectivity analyses were conducted to examine intrinsic correlations between three proposed subnetworks (sensory/discriminative, affective/motivational, and cognitive/evaluative) involved in pain processing. Results. The percept-related model captured more extensive activation than the stimulus-related model and demonstrated an association between higher subjective pain and activation in expected cortical (dorsolateral prefrontal cortex, ventrolateral prefrontal cortex, insula, dorsal anterior cingulate cortex [dACC] extending into pre-supplementary motor area) and subcortical (thalamus, striatum) areas. Moreover, connectivity results supported the posited roles of dACC and insula as key relay sites during neural processing of subjective pain. In particular, anterior insula appeared to link sensory/discriminative regions with regions in the other subnetworks, and dACC appeared to serve as a hub for affective/motivational, cognitive/evaluative, and motor subnetworks. Conclusions. Using a percept-related model, brain regions involved in the processing of subjective pain during the application of cold stimuli were identified. Connectivity analyses identified linkages between key subnetworks involved in processing subjective pain. [ABSTRACT FROM AUTHOR]

In this study, we wished to examine the relationship between the structural connectivity of the fornix, a white matter (WM) tract in the limbic system, which is affected in amnestic mild cognitive impairment (aMCI) and Alzheimer's disease, and the resting-state functional connectivity (FC) of two key related subcortical structures, the thalamus, and hippocampus. Twenty-two older healthy controls (HC) and 18 older adults with aMCI underwent multi-modal MRI scanning. The fornix was reconstructed using constrained-spherical deconvolution-based tractography. The FC between the thalamus and hippocampus was calculated using a region-of-interest approach from which the mean time series were exacted and correlated. Diffusion tensor imaging measures of theWM microstructure of the fornix were correlated against the Fisher Z correlation values from the FC analysis. There was no difference between the groups in the fornix WM measures, nor in the resting-state FC of the thalamus and hippocampus. We did however find that the relationship between functional and structural connectivity differed significantly between the groups. In the HCs, there was a significant positive association between linear diffusion (CL) in the fornix and the FC of the thalamus and hippocampus, however, there was no relationship between these measures in the aMCI group. These preliminary findings suggest that in aMCI, the relationship between the functional and structural connectivity of regions of the limbic system may be significantly altered compared to healthy ageing. The combined use of diffusion weighted imaging and functional MRI may advance our understanding of neural network changes in aMCI, and elucidate subtle changes in the relationship between structural and functional brain networks. [ABSTRACT FROM AUTHOR]

New Findings What is the central question of this study? It is widely reported that non-painful, local warming of the skin elicits highly reproducible vasodilatation in young healthy individuals. Systemic hypoxia also elicits cutaneous vasodilatation, although this is modest in comparison to that elicited by skin heating. The interaction of simultaneous cutaneous local thermal hyperaemia and systemic hypoxia has not been investigated., What is the main finding and its importance? When compared with normoxia, systemic hypoxaemia enhances skin vasodilator capacity in response to local skin warming. This finding has important implications for understanding the physiology of skin microvascular reactivity in individuals exposed to systemic hypoxia or with a hypoxic microenvironment of the skin., The primary aim of this study was to investigate the effect of systemic poikilocapnic hypoxia on forearm cutaneous thermal hyperaemia. A secondary aim was to examine the relationship between the individual susceptibility to oxygen desaturation and cutaneous vasodilator capacity. Twelve healthy participants (seven male) were exposed to 9 h of normoxia and 12% poikilocapnic hypoxia in a temperature- and humidity-controlled environmental chamber. Skin blood flow was assessed at the ventral forearm using laser Doppler flowmetry combined with rapid local heating. After 6 min at baseline (skin temperature clamped at 33°C), local skin temperature was elevated at a rate of 0.5°C every 5 s up to 42°C to elicit a sensory axon response and then held constant for 30 min to cause a plateau. Skin blood flow was calculated as cutaneous vascular conductance [CVC; in perfusion units/mean arterial blood pressure (APU mmHg−1)] and expressed in raw format and relative to heating at 44°C in normoxia (%CVC44). During hypoxaemia, vasodilatation was greater during the initial peak (raw, Δ0.35 APU mmHg−1, P = 0.09; %CVC44, Δ18%, P = 0.05) and the plateau phase (raw, Δ0.55 APU mmHg−1, P = 0.03; %CVC44, Δ26%, P = 0.02). The rate of rise in cutaneous blood flow during the initial peak was significantly greater during poikilocapnic hypoxia ( P < 0.01). We observed a negative relationship between oxygen saturation in poikilocapnic hypoxia and the change in baseline ( P = 0.06), initial peak ( P = 0.01) and plateau phase of thermal hyperaemia ( P = 0.01). Prolonged poikilocapnic hypoxia causes robust increases in CVC during both phases of thermal hyperaemia that are dependent on the oxygen saturation of the individual. [ABSTRACT FROM AUTHOR]

Objective The study was undertaken to determine whether normobaric hypoxia causes elevated brain volume and intracranial pressure in individuals with symptoms consistent with acute mountain sickness (AMS). Methods Thirteen males age = (26 (sd 6)) years were exposed to normobaric hypoxia (12% O2) and normoxia (21% O2). After 2 and 10 hours, AMS symptoms were assessed alongside ventricular and venous vessel volumes, cerebral blood flow, regional brain volumes, and intracranial pressure, using high-resolution magnetic resonance imaging. Results In normoxia, neither lateral ventricular volume ( R2 = 0.07, p = 0.40) nor predominance of unilateral transverse venous sinus drainage ( R2 = 0.07, p = 0.45) was related to AMS symptoms. Furthermore, despite an increase in cerebral blood flow after 2 hours of hypoxia (hypoxia vs normoxia: Δ148ml/min−1, 95% confidence interval [CI] = 58 to 238), by 10 hours, when AMS symptoms had developed, cerebral blood flow was normal (Δ−51ml/min−1, 95% CI = −141 to 39). Conversely, at 10 hours brain volume was increased (Δ59ml, 95% CI = 8 to 110), predominantly due to an increase in gray matter volume (Δ73ml, 95% CI = 25 to 120). Therefore, cerebral spinal fluid volume was decreased (Δ−40ml, 95% CI = −67 to −14). The intracranial pressure response to hypoxia varied between individuals, and as hypothesized, the most AMS-symptomatic participants had the largest increases in intracranial pressure (AMS present, Δ7mmHg, 95% CI = −2.5 to 17.3; AMS not present, Δ−1mmHg, 95% CI = −3.3 to 0.5). Consequently, there was a significant relationship between the change in intracranial pressure and AMS symptom severity ( R2 = 0.71, p = 0.002). Interpretation The data provide the strongest evidence to date to support the hypothesis that the 'random' nature of AMS symptomology is explained by a variable intracranial pressure response to hypoxia. ANN NEUROL 2014;75:890-898 [ABSTRACT FROM AUTHOR]

Beauty is in the eye of the beholder. How attractive someone is perceived to be depends on the individual or cultural standards to which this person is compared. But although comparisons play a central role in the way people judge the appearance of others, the brain processes underlying attractiveness comparisons remain unknown. In the present experiment, we tested the hypothesis that attractiveness comparisons rely on the same cognitive and neural mechanisms as comparisons of simple nonsocial magnitudes such as size. We recorded brain activity with functional magnetic resonance imaging (fMRI) while participants compared the beauty or height of two women or two dogs. Our data support the hypothesis of a common process underlying these different types of comparisons. First, we demonstrate that the distance effect characteristic of nonsocial comparisons also holds for attractiveness comparisons. Behavioral results indicated, for all our comparisons, longer response times for near than far distances. Second, the neural correlates of these distance effects overlapped in a frontoparietal network known for its involvement in processing simple nonsocial quantities. These results provide evidence for overlapping processes in the comparison of physical attractiveness and nonsocial magnitudes. [ABSTRACT FROM AUTHOR]