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24.04.2026, Friday, 16:00-17:30
This workshop proposes an integrative perspective on pain as an emergent property of a distributed nociceptive system, building on the conceptual framework introduced by Robert C. Coghill. Rather than being encoded locally or linearly, nociceptive signals are integrated across space and time, giving rise to hallmark features of pain perception such as nonlinearity and disproportionality. The workshop will examine how temporal and spatial dimensions of stimulation can be functionally exchanged—trading time with space—to shape pain in humans.
Opening with a keynote by Robert C. Coghill, the workshop will outline the distributed nociceptive system framework and its implications for understanding pain variability, hyperalgesic and hypoalgesic modulations of pain. Subsequent talks will present psychophysical signatures of this framework across temporal and spatial domains. Temporal modulation will be addressed through offset analgesia (J. Poehlmann), demonstrating how small decreases in stimulus intensity evoke disproportionately large reductions in perceived pain. This phenomenon will be discussed as an expression of temporal contrast computation, reflecting the system’s sensitivity to changes over time rather than absolute input levels, and its generalisability across modalities, and experimental contexts. Spatial modulation will be addressed through spatial summation and lateral inhibition (W.M. Adamczyk), demonstrating how pain intensity reflects nonlinear integration of distributed nociceptive inputs, in which increasing stimulated area can paradoxically amplify or suppress pain as a function of spatial configuration, inter-site interactions, and attentional selection of nociceptive subregions. The thermonociceptive illusions, such as the Thermal Grill and Paradoxical Heat Sensation (A. Mitchell) will be examined as a canonical case of emergent nociceptive perception, in which spatially and temporally interleaved innocuous warm and cool inputs are integrated across populations of thermosensory and nociceptive neurons, producing a pain percept that cannot be attributed to any single stimulation site and instead reflects distributed spatial contrast computations.
Across paradigms, the workshop will emphasize shared computational principles, including contrast enhancement, distributed integration, and attentional mediation. By bridging classical psychophysics with contemporary systems neuroscience, this symposium aims to provide a unifying mechanistic framework for spatial and temporal pain modulation, stimulate novel experimental approaches, and advance understanding of pain processing in both health and disease—making it highly relevant for the Neuronus IBRO Forum audience.
Pediatric Pain Research Center, Cincinnati Children’s Hospital; Division of Behavioral Medicine and Clinical Psychology, Cincinnati Children’s Hospital; Department of Pediatrics, University of Cincinnati College of Medicine
"Distributed Nociceptive System Framework and its Implications for Understanding Pain Variability, Hyperalgesic and Hypoalgesic Modulations of Pain"
A new overarching conceptual framework for understanding pain, termed the Distributed Nociceptive System (DNS), integrates two neglected concepts - population coding and distributed processing. The central tenet of this framework is that the extraction and utilization of nociceptive information is a process that can be accomplished separately and largely independently by populations of neurons across multiple sites within the central nervous system. As such, processing of nociceptive information can occur in a highly distributed fashion, yielding a system that is very resistant to disruption. The DNS provides a bridge between the basic neuroscience and clinical worlds by providing a mechanistic framework for developing an understanding of the perplexing symptoms of chronic pain. For example, altered receptive field tuning may result in enhanced recruitment of nociceptive neurons and spread of pain. Thus, examining systems supporting spatial tuning may provide important insights into how pain can spread and how this spread can be reversed. Moreover, the widely distributed brain systems that are involved in the construction of the pain experience may require distributed regulation to instantiate either positive or negative changes.
Aarhus University, Aarhus, Denmark
"Thermo-nociceptive illusions in humans"
Thermo-nociceptive illusions, unusual thermosensory or painful experiences arising from the integration of warm and cold signals, have intrigued researchers for decades. In this talk, I will present our recent work on two such phenomena. The Thermal Grill Illusion (TGI), is characterised by a burning or painful heat sensation when warm and cold stimuli are spatially interleaved on the skin. In contrast, Paradoxical Heat Sensation (PHS) refers to the experience of warmth or heat pain during cooling, induced by temporally alternating warm and cold. I will show that the TGI is driven by the integration of thermal signals within both the spinal cord and the brain. I will argue that contrast is a shared mechanisim got both illusions, while emphasising marked individual differences in perceptual experience. These findings reveal how thermonociceptive illusions provide a window onto normal thermosensory processing, highlighting the importance of understanding thermosensory integration within the central nervous system.
Academy of Physical Education, Katowice, Poland
"Spatial summation of nociceptive input and its limits"
Pain is not a simple sum of nociceptive inputs. Instead, spatial interactions between stimulated body regions fundamentally shape how pain is perceived, leading to nonlinearity and disproportionality in pain reports. In this talk, I will discuss recent psychophysical evidence demonstrating how two core spatial mechanisms—spatial summation and lateral inhibition—interact to modulate pain intensity. I argue that these mechanisms cannot be fully explained by peripheral or spinal processes alone, but rather reflect higher-order integration of spatial information. Importantly, I will highlight emerging evidence suggesting that attention mediates spatial pain modulation. This selective amplification or suppression of nociceptive signals depends on task demands and spatial focus. Together, these findings suggest that spatial pain processing is dynamic and context-dependent, rather than fixed sensory encoding. This has important implications for understanding pain modulation in both health and disease.
University of Lübeck, Lübeck, Germany
"Temporal contrast enhancement in pain"
Temporal properties of pain modulation can be investigated using several psychophysical paradigms, one prominent example being offset analgesia. In this phenomenon, a minor decrease in stimulus intensity leads to a disproportionately large reduction in perceived pain, a response thought to be mediated by temporal filtering mechanisms that enhance contrast between small changes in sensory input over time. Similar temporal filtering processes have been documented across multiple sensory domains, raising the possibility that offset analgesia reflects a modality-general mechanism of temporal contrast enhancement rather than a pain-specific phenomenon. In this talk, we will review recent work from our laboratory supporting this view, combining psychophysical and neurophysiological evidence for temporal contrast enhancement in auditory stimulation, and discuss modality-dependent differences in temporal modulation that point to distinct, modality-specific processing patterns.
Department of Cellular Neurophysiology, Medical School OWL, Bielefeld University, Bielefeld, Germany, International Max Planck Research School for Neurosciences, Göttingen, Germany
"Estrogenic Regulation of Human Nociceptor Excitability: A Cellular Platform to Study Hormonal Mechanisms in Migraine"
Migraine is the most common severe primary headache with a strong sex bias, affecting women 2-3 times more frequently than men. Fluctuations in estrogen levels contribute to migraine susceptibility, yet the cellular mechanisms behind it remain incompletely understood. Human and rodent nociceptors exhibit greater molecular diversity than previously recognized. Therefore, human-derived cellular models are necessary to study pain disorders such as migraine.
This study aimed to differentiate human dermal fibroblasts (HDFa)-derived induced Pluripotent Stem Cells (iPSCs) into peptidergic nociceptive neurons. Secondly, it assessed the influence of phenol red (PR) present in cell culture medium, on neuronal differentiation, in order to consider sources of unintended estrogenic activity in cell cultures. Moreover, we tested the impact of supplemented estrogen on neuronal excitability.
HDFa-derived iPSCs were differentiated into nociceptors in PR-containing medium, PR-free (PR-) medium, or PR- medium supplemented with 17β-estradiol (E2). Neuronal differentiation was assessed by expression of nociceptor markers and electrophysiological characterization. Whole-cell patch-clamp recordings were performed to evaluate action potential firing and membrane currents.
The differentiated cells expressed neuronal markers TUJ1 and ISL1 and peptidergic markers CGRP, SCN11A, TRKA and TRPV1. Cells differentiated in the medium containing PR, known to have affinity for estrogen receptors, exhibited the highest excitability. Supplementation of PR- medium with E2 increased neuronal excitability compared to PR- medium alone.
These findings demonstrate that estrogenic conditions, also unintended, influence nociceptor differentiation and neuronal excitability. This human-derived platform can be utilized as an in vitro model of trigeminal ganglion neurons for further investigation of migraine pathophysiology and sex specific differences.
