Pain
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Randomized Controlled Trial
Noninvasive neuromodulation of subregions of the human insula differentially affect pain processing and heart-rate variability: a within-subjects pseudo-randomized trial.
The insula is an intriguing target for pain modulation. Unfortunately, it lies deep to the cortex making spatially specific noninvasive access difficult. Here, we leverage the high spatial resolution and deep penetration depth of low-intensity focused ultrasound (LIFU) to nonsurgically modulate the anterior insula (AI) or posterior insula (PI) in humans for effect on subjective pain ratings, electroencephalographic (EEG) contact heat-evoked potentials, as well as autonomic measures including heart-rate variability (HRV). ⋯ Low-intensity focused ultrasound to PI affected earlier EEG amplitudes, whereas LIFU to AI affected later EEG amplitudes. Only LIFU to the AI affected HRV as indexed by an increase in SD of N-N intervals and mean HRV low-frequency power. Taken together, LIFU is an effective noninvasive method to individually target subregions of the insula in humans for site-specific effects on brain biomarkers of pain processing and autonomic reactivity that translates to reduced perceived pain to a transient heat stimulus.
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Recent evidence highlights the importance of the neuroimmune interface, including periphery-to-central nervous system (CNS) neuroimmune crosstalk, in chronic pain. Although neuroinflammatory processes have been implicated in central sensitization for a long time, their potential neuroprotective and analgesic effects remain relatively elusive. We have explored the relationships between cytokine expression and symptom severity, and candidates for periphery-to-CNS crosstalk. ⋯ The cytokines CCL11, CD5, IL8, and MMP-10 were elevated in the CSF, had positive correlations between CSF and serum levels, and associated in a nonlinear manner with back, but not leg, pain intensity in the LDH, but not the DDD, group. In conclusion, we found evidence for neuroimmune activation in the CNS of both patient groups in the absence of systemic inflammation and signs of a communication between CSF and serum. Complex and disease-specific associations were found between cytokines in CSF and back pain intensity.
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Chronic pain affects individuals' work participation. The impact of chronic pain on work has historically been measured through sickness absence, though it is now appreciated that the impacts on work are far wider. This mixed-methods review aimed to identify the full range of impacts of pain on work in addition to impacts that are currently measured quantitatively to inform the development of a new questionnaire assessing the wider impacts of chronic pain on work. ⋯ Quantitative measures mainly assessed impacts related to the quantity and quality of work (29 of 42 measures). Seventeen aspects were only discussed within the qualitative literature. This study identifies a discrepancy between the impacts that have been the focus of quantitative measures and the range that individuals working with chronic pain experience and highlights the need for a new measure assessing a wider range of issues.
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Growing evidence has suggested that time-varying functional connectivity between different brain regions might underlie the dynamic experience of pain. This study used a novel, data-driven framework to characterize the dynamic interactions of large-scale brain networks during sustained pain by estimating recurrent patterns of phase-synchronization. Resting-state functional magnetic resonance imaging signals were collected from 50 healthy participants before (once) and after (twice) the onset of sustained pain that was induced by topical application of capsaicin cream. ⋯ These changes can account for the perceived pain intensity and reported unpleasantness induced by capsaicin application. In contrast, state 3, characterized by phase-synchronization between the cognitive control network and sensory networks, decreased after the onset of sustained pain. These results are indicative of a shift toward internally directed self-referential processes (state 1) and away from externally directed cognitive control processes (state 3) during sustained pain.