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Horing, B.

Publications and source records attributed to Horing, B..

4 recordsLinked to original sources

Conditioned pain modulation recruits the descending pain modulatory system to inhibit spinal activity

Conditioned pain modulation (CPM) is a phenomenon where the perception of pain is reduced in the presence of a second painful stimulus. In rodents, a similar phenomenon involves descending control pathways that rely on the brainstem to modulate spinal cord activity while in humans, descending mechanisms including the spinal cord remain elusive. In this study, we applied functional MRI to simultaneously record brain and spinal cord responses during CPM in healthy participants. CPM developed over time and was associated with reduced activity in key pain-related brain regions and the spinal cord dorsal horn. Conversely, regions involved in descending pain modulation showed increased activity during CPM. Functional connectivity analyses revealed reduced coupling during CPM between spinal and descending control regions. Our findings demonstrate that CPM involves both the descending pain control system to inhibit spinal activity and bottom-up pain signalling of attenuated spinal responses.

neuroscience↗

Agency and Expectations in Pain Treatment: An Investigation of the Active Inference Model

The fact that we cannot tickle ourselves is traditionally explained by the attenuation of somatosensation by predictions from a forward model of self-generated movements. Alternatively, it has been suggested within the framework of active inference that Bayes-optimal reduction of sensory precision can explain this phenomenon. Combining a pain paradigm with stimulus-related expectations allows to compare both models through predictions from the Bayesian account of expectation-based hypoalgesia, where pain is influenced by the precisions of somatosensation and expectation. In two experiments, heat pain was sham-treated either externally or by the subject, while a cue created higher or lower treatment expectations. Both experiments revealed greater pain relief under self-treatment and high treatment expectations. Electroencephalography revealed a modulation of theta-to-beta frequencies linked to agency and top-down modulations of pain perception. Computational modeling showed that this is better explained by an attenuation of somatosensation than a downregulation of somatosensation precision, favoring the forward model.

neuroscience↗

Pain-related learning signals in the human insula

Pain is not only a perceptual phenomenon, but also a preeminent learning signal. In reinforcement learning models, prediction errors (PEs) play a crucial role, i.e. the mismatch between expectation and sensory input. In particular, advanced learning models require the representation of different types of PEs, namely signed PEs (whether more or less pain was expected) to specify the direction of learning, and unsigned PEs (the absolute deviation from an expectation) to adapt the learning rate. The insula has been shown to play an important role in pain intensity coding and in signaling surprise. However, mainly unsigned PEs could be identified in the anterior insula. It remains an open question whether these PEs are specific to pain, and whether signed PEs are also represented in the insula. To answer these questions, 47 subjects learned associations of two conditioned stimuli (CS) with four unconditioned stimuli (US; painful heat or loud sound, of one low and one high intensity each) while undergoing functional magnetic resonance imaging (fMRI) and skin conductance response (SCR) measurements. CS-US associations reversed multiple times between intensities and between sensory modalities, generating frequent PEs. SCRs indicated comparable nonspecific characteristics of the two modalities. fMRI analyses focusing on the insular and opercular cortices contralateral to painful stimulation showed that activation in the anterior insula correlated with unsigned intensity PEs. Importantly, this unsigned PE signal was similar for pain and aversive sounds and also modality PEs, indicating an unspecific aversive surprise signal. Conversely, signed pain intensity PE signals were modality-specific and located in the dorsal posterior insula, an area previously implicated in pain intensity processing. Previous studies have identified abnormal insula function and abnormal learning as potential causes of pain chronification. Our findings link these results and suggest one potential mechanism, namely a misrepresentation of learning relevant prediction errors in the insular cortex.

neuroscience↗

The parietal operculum preferentially encodes heat pain and not salience

Substantial controversy exists as to which part of brain activity is genuinely attributable to pain-related percepts, and which activity is due to general aspects of sensory stimulation, such as its salience, or the accompanying arousal. The challenge posed by this question rests largely in the fact that pain per se exhibits highly intense but unspecific characteristics. These therefore should be matched by potential control conditions. Here, we used a unique combination of functional magnetic resonance imaging, behavioral and autonomic measures to address this longstanding debate in pain research.\n\nSubjects rated perceived intensity in a sequence alternating between heat and sound stimuli. Neuronal activity was monitored using fMRI. Either modality was presented in six different intensities, three of which lay above the pain threshold (for heat) or the unpleasantness threshold (for sound). We performed our analysis on 26 volunteers in which psychophysiological responses (as per skin conductance responses) did not differ between the two stimulus modalities. Having thus ascertained a comparable amount of stimulation-related but unspecific activation, we analyzed stimulus response functions after painful stimulation, and contrasted them with those of the matched acoustic control condition. Furthermore, analysis of fMRI data was performed on the brain surface to circumvent blurring issues stemming from the close proximity of several regions of interest located in heavily folded cortical areas. We focused our analyses on insular and periinsular regions which are strongly involved in processing of painful stimuli. We employed an axiomatic approach to determine areas showing higher activation in painful compared to non-painful heat, and at the same time showing a steeper stimulus response function for painful heat as compared to unpleasant sound. Intriguingly, an area in the posterior parietal operculum emerged whose response showed a pain preference after satisfying all axiomatic constraints.\n\nThis result has important implications for the interpretation of functional imaging findings in pain research, as it clearly demonstrates that there are areas whose activity following painful stimulation is not due to general attributes or results of sensory stimulation, such as salience or arousal. Conversely, several areas did not conform to the formulated axioms to rule out general factors as explanations.

neuroscience↗