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      Altered functional connectivity density in patients with herpes zoster and postherpetic neuralgia

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          The aim of this study was to explore intrinsic functional connectivity patterns in patients with herpes zoster (HZ) and postherpetic neuralgia (PHN).

          Patients and methods

          Thirty-three right-handed HZ patients (13 males; mean age 57.15±9.30 years), 22 right-handed PHN patients (9 males; mean age 66.13±6.77 years), and 28 well-matched healthy controls (HC) (9 males; mean age 54.21±7.72 years) underwent resting-state functional magnetic resonance imaging for intrinsic functional connectivity analyses. Functional connectivity density (FCD) was calculated and compared among the PHN, HZ, and HC groups. In addition, the Pearson correlation coefficient was calculated to compare various clinical indices in the regions with abnormal FCD values.


          Compared with the HC, both HZ and PHN patients showed significantly decreased FCD in the precuneus, and patients with HZ displayed significantly increased FCD in the brainstem/limbic lobe/parahippocampalgyrus, whereas patients with PHN displayed significantly increased FCD in the hippocampus (correlation thresholds r=0.25, voxel level of P<0.01 and Gaussian random field theory at a cluster level of P<0.05). However, the FCD was not significantly different between the PHN and HZ patients. Furthermore, the decreased FCD in the precuneus was positively correlated with the visual analog scale score in the PHN group ( r=0.672; P=0.001).


          Decreased connectivity of the precuneus occurred in both HZ and PHN patients, indicating a disrupted default-mode network. Furthermore, in the HZ group (initial stage of the virus infection), hyperconnectivity was observed in systems involved in pain transmission and interpretation, but hyperconnectivity only occurred in the hippocampus in the PHN group (neuropathic pain stage).

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          Most cited references 31

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          Shape shifting pain: chronification of back pain shifts brain representation from nociceptive to emotional circuits.

          Chronic pain conditions are associated with abnormalities in brain structure and function. Moreover, some studies indicate that brain activity related to the subjective perception of chronic pain may be distinct from activity for acute pain. However, the latter are based on observations from cross-sectional studies. How brain activity reorganizes with transition from acute to chronic pain has remained unexplored. Here we study this transition by examining brain activity for rating fluctuations of back pain magnitude. First we compared back pain-related brain activity between subjects who have had the condition for ∼2 months with no prior history of back pain for 1 year (early, acute/subacute back pain group, n = 94), to subjects who have lived with back pain for >10 years (chronic back pain group, n = 59). In a subset of subacute back pain patients, we followed brain activity for back pain longitudinally over a 1-year period, and compared brain activity between those who recover (recovered acute/sub-acute back pain group, n = 19) and those in which the back pain persists (persistent acute/sub-acute back pain group, n = 20; based on a 20% decrease in intensity of back pain in 1 year). We report results in relation to meta-analytic probabilistic maps related to the terms pain, emotion, and reward (each map is based on >200 brain imaging studies, derived from neurosynth.org). We observed that brain activity for back pain in the early, acute/subacute back pain group is limited to regions involved in acute pain, whereas in the chronic back pain group, activity is confined to emotion-related circuitry. Reward circuitry was equally represented in both groups. In the recovered acute/subacute back pain group, brain activity diminished in time, whereas in the persistent acute/subacute back pain group, activity diminished in acute pain regions, increased in emotion-related circuitry, and remained unchanged in reward circuitry. The results demonstrate that brain representation for a constant percept, back pain, can undergo large-scale shifts in brain activity with the transition to chronic pain. These observations challenge long-standing theoretical concepts regarding brain and mind relationships, as well as provide important novel insights regarding definitions and mechanisms of chronic pain.
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            Functional connectivity density mapping.

            Brain networks with energy-efficient hubs might support the high cognitive performance of humans and a better understanding of their organization is likely of relevance for studying not only brain development and plasticity but also neuropsychiatric disorders. However, the distribution of hubs in the human brain is largely unknown due to the high computational demands of comprehensive analytical methods. Here we propose a 10(3) times faster method to map the distribution of the local functional connectivity density (lFCD) in the human brain. The robustness of this method was tested in 979 subjects from a large repository of MRI time series collected in resting conditions. Consistently across research sites, a region located in the posterior cingulate/ventral precuneus (BA 23/31) was the area with the highest lFCD, which suggest that this is the most prominent functional hub in the brain. In addition, regions located in the inferior parietal cortex (BA 18) and cuneus (BA 18) had high lFCD. The variability of this pattern across subjects was <36% and within subjects was 12%. The power scaling of the lFCD was consistent across research centers, suggesting that that brain networks have a "scale-free" organization.
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              Pain and the brain: specificity and plasticity of the brain in clinical chronic pain.


                Author and article information

                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                27 April 2018
                : 11
                : 881-888
                [1 ]Department of Radiology, The First Affiliated Hospital, Nanchang University, Nanchang, Jiangxi, People’s Republic of China
                [2 ]Department of Pain, The First Affiliated Hospital, Nanchang University, Nanchang, Jiangxi, People’s Republic of China
                Author notes
                Correspondence: Jian Jiang, Department of Radiology, The First Affiliated Hospital, Nanchang University, 17 Yongwaizheng Street, Nanchang, Jiangxi 330006, People’s Republic of China, Tel +86 791 8869 3825, Email jij2002cn@ 123456126.com

                These authors contributed equally to this work

                © 2018 Hong et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Original Research


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