Neural circuitry mediating inflammation-induced central pain amplification in human experimental endotoxemia

Benson, Sven; Rebernik, Laura; Kleine-Borgmann, Julian; Engler, Harald; Schlamann, Marc; Forsting, Michael; Schedlowski, Manfred; Elsenbruch, Sigrid

doi:10.1016/j.bbi.2015.03.017

Cited by 49 publications

(51 citation statements)

References 58 publications

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“…This study identified a specific increase in left anterior insula to left mid-cingulate cortex that additionally predicted LPS associated back pain and global sickness [42]. These regions form key components of the pain matrix, and it is noteworthy that they have also been previously linked to LPS induced increases in visceral pain sensitivity [153].…”

Section: Network Connectivitymentioning

confidence: 97%

Brain Structures Implicated in Inflammation-Associated Depression

Harrison

2016

Current Topics in Behavioral Neurosciences

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Systemic inflammation rapidly impairs mood, motivation, and cognition inducing a stereotyped cluster of symptoms collectively known as "sickness behaviors." When inflammation is severe or chronic, these behavioral changes can appear indistinguishable from major depressive disorder (MDD). Human and rodent neuroimaging combined with experimental inflammatory challenges has clarified the neural circuitry associated with many of the key features of inflammation-induced-sickness behavior, and in so doing revealed often-remarkable commonalities with circuit abnormalities observed in MDD. This review aims to provide the first synthesis of this work illustrating areas of convergence and divergence with the MDD literature as well as highlighting areas for future study.

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Section: Network Connectivitymentioning

confidence: 97%

Brain Structures Implicated in Inflammation-Associated Depression

Harrison

2016

Current Topics in Behavioral Neurosciences

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“…An increased responsiveness of the insula to interoceptive signals would, therefore, make individuals more prone to feeling fatigued. Interestingly, it has repeatedly been shown that inflammation increases insular activity (121, 122, 125–127). Two studies even show a relationship between inflammation-induced insular function and fatigue development (122, 126).…”

Section: Potential Neuronal Mechanisms Underlying Dimensions Of Inflamentioning

confidence: 99%

Role of Inflammation in Human Fatigue: Relevance of Multidimensional Assessments and Potential Neuronal Mechanisms

2017

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Fatigue is a highly disabling symptom in various medical conditions. While inflammation has been suggested as a potential contributor to the development of fatigue, underlying mechanisms remain poorly understood. In this review, we propose that a better assessment of central fatigue, taking into account its multidimensional features, could help elucidate the role and mechanisms of inflammation in fatigue development. A description of the features of central fatigue is provided, and the current evidence describing the association between inflammation and fatigue in various medical conditions is reviewed. Additionally, the effect of inflammation on specific neuronal processes that may be involved in distinct fatigue dimensions is described. We suggest that the multidimensional aspects of fatigue should be assessed in future studies of inflammation-induced fatigue and that this would benefit the development of effective therapeutic interventions.

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“…In addition, the HPA axis influences the activations of the abovementioned brain regions under acute pain conditions. For instance, previous studies demonstrated that elevated cortisol levels were (1) associated with reduced pain unpleasantness and decreased pain-related brain activation during constant noxious stimulation [22], (2) linked with lower pain threshold and stronger PFC activity in response to inflammation-induced pain [58], and (3) related to enhanced hippocampal activation during step-up noxious stimulation (an increasing pattern of noxious stimulation) [59]. These studies suggested that acute pain, acting in a similar way with acute stress, may evoke cortisol levels to boost the survival of the organism by inhibiting and/or facilitating activities of related brain networks.…”

Section: Neural Plasticity In Acute and Chronic Painmentioning

confidence: 99%

The Role of Stress Regulation on Neural Plasticity in Pain Chronification

2016

Neural Plasticity

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Pain, especially chronic pain, is one of the most common clinical symptoms and has been considered as a worldwide healthcare problem. The transition from acute to chronic pain is accompanied by a chain of alterations in physiology, pathology, and psychology. Increasing clinical studies and complementary animal models have elucidated effects of stress regulation on the pain chronification via investigating activations of the hypothalamic-pituitary-adrenal (HPA) axis and changes in some crucial brain regions, including the amygdala, prefrontal cortex, and hippocampus. Although individuals suffer from acute pain benefit from such physiological alterations, chronic pain is commonly associated with maladaptive responses, like the HPA dysfunction and abnormal brain plasticity. However, the causal relationship among pain chronification, stress regulation, and brain alterations is rarely discussed. To call for more attention on this issue, we review recent findings obtained from clinical populations and animal models, propose an integrated stress model of pain chronification based on the existing models in perspectives of environmental influences and genetic predispositions, and discuss the significance of investigating the role of stress regulation on brain alteration in pain chronification for various clinical applications.

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Neural circuitry mediating inflammation-induced central pain amplification in human experimental endotoxemia

Cited by 49 publications

References 58 publications

Brain Structures Implicated in Inflammation-Associated Depression

Brain Structures Implicated in Inflammation-Associated Depression

Role of Inflammation in Human Fatigue: Relevance of Multidimensional Assessments and Potential Neuronal Mechanisms

The Role of Stress Regulation on Neural Plasticity in Pain Chronification

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