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Zunhammer, M.

Publications and source records attributed to Zunhammer, M..

3 recordsLinked to original sources

Meta-analytic evidence for distinct neural correlates of conditioned vs. verbally induced placebo analgesia

Placebo analgesia demonstrates that belief and expectation can significantly alter pain, even without active treatment. Placebo analgesia can be induced through verbal suggestion, classical conditioning, or their combination, though the role of conditioned neural responses above and beyond effects of verbal instructions remains unclear. We conducted a systematic meta-analysis of individual participant data from 16 within-participant placebo neuroimaging studies (n = 409), employing univariate and multivariate analyses to identify shared and distinct mechanisms of placebo analgesia induced by suggestions alone versus suggestions combined with conditioning. Both techniques increased activity during pain in the dorsolateral prefrontal and inferior parietal cortices and decreased activation in the insula, putamen, and primary sensory areas. Adding conditioning enhanced engagement of regions associated with context representation and pain modulation (e.g., dorsolateral/dorsomedial prefrontal cortices) and decreases in nociceptive regions (e.g., primary sensory and insular areas). Conditioning also strengthened the association between analgesia and nociceptive activity, as reflected in the Neurologic Pain Signature. Combining conditioning with instructions yielded greater analgesia, mediated by increased ventromedial prefrontal and dorsal caudate activity, alongside decreased sensory-nociceptive and cerebellar activity. These findings suggest the two strategies rely on partially distinct mechanisms, which could be combined to optimize placebo analgesias clinical application.

neuroscience↗

Gray matter cortical thickness predicts individual pain sensitivity: a multi-center machine learning approach

Pain sensitivity is known to considerably vary across individuals. While the variability in pain has been linked to structural neural correlates, it is still unclear how well these findings replicate in independent data and whether they are powerful enough to provide reliable pain sensitivity predictions on the individual level. In this study, we constructed a predictive model of pain sensitivity utilising structural MRI-based cortical thickness data from a multi-center dataset (3 centers, 131 healthy participants). Cross-validated estimates revealed a statistically significant and clinically relevant predictive performance (Pearsons r = 0.36, p < 0.0005). The predictions were found to be specific to pain sensitivity and not biased towards potential confounding effects (e.g., anxiety, stress, depression, center-effects). Analysis of model coefficients suggests that the most robust cortical thickness predictors of pain sensitivity are the right rostral anterior cingulate gyrus, left parahippocampal gyrus and left temporal pole. Cortical thickness in these regions was negatively correlated to pain sensitivity. Our results can be considered as a proof-of-concept for the capacity of brain morphology to predict pain sensitivity, paving the way towards future multimodal brain-based biomarkers of pain. HighlightsO_LIWe present a robust, brain structure-based multi-center predictive model for pain sensitivity. C_LIO_LIOur model based on gray matter cortical thickness explains 13% of the variance in pain sensitivity and generalizes to out-of-center data. C_LIO_LIThe predictions are specific to pain sensitivity and not driven by potential confounders such as stress, depression, anxiety, and center-effects. C_LIO_LIThe most important predictors were rostral anterior cingulate cortex, parahippocampal gyrus and temporal pole, all negatively correlated with pain sensitivity. C_LI

neuroscience↗

Pain-free resting-state functional brain connectivity predicts individual pain sensitivity

Individual differences in pain perception are of key interest in basic and clinical research as altered pain sensitivity is both a characteristic and a risk factor for many pain conditions. It is, however, unclear how individual susceptibility to pain is reflected in the pain-free resting-state brain activity and functional connectivity.\n\nHere, we identified and validated a network pattern in the pain-free resting-state functional brain connectome that is predictive of interindividual differences in pain sensitivity. Our predictive network signature (https://spisakt.github.io/RPN-signature) allows assessing the individual susceptibility to pain without applying any painful stimulation, as might be valuable in patients where reliable behavioural pain reports cannot be obtained. Additionally, as a direct, non-invasive readout of the supraspinal neural contribution to pain sensitivity, it may have broad implications for translational research and the development and assessment of analgesic treatment strategies.

neuroscience↗