Scaling Up Cortical Control Inhibits Pain

Dale, Jahrane; Zhou, Haocheng; Zhang, Qiaosheng; Martinez, Erik; Hu, Sile; Liu, Kevin; Urien, Louise; Chen, Zhe; Wang, Jing

doi:10.1016/j.celrep.2018.03.139

Cited by 70 publications

(104 citation statements)

References 39 publications

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“…4c–e ). These results confirm the finding that chronic pain induces an anatomically nonspecific increase in aversion 8 , 30 . When we injected ketamine into these rats, we did not observe long-lasting anti-nociceptive effects, as manifested by only a transient relief of mechanical allodynia (Fig.…”

Section: Resultssupporting

confidence: 91%

“…Our results here extend beyond these results to show that chronic pain at one site in the body can increase the aversive response to acute mechanical pain from a different location. These results are compatible with two previous studies on the evaluation of aversive responses in rodents to thermal and mechanical noxious stimulations in the chronic pain state 8 , 30 . These results in animal models confirm the epidemiological findings in clinical pain syndromes, such as fibromyalgia and persistent postoperative pain 2 – 6 .…”

Section: Discussionsupporting

confidence: 93%

“…In contrast to the ACC, an adjacent area in the rodent cortex, the prelimbic PFC (PL-PFC) is known to provide pain inhibition when activated 26 , 51 . Interestingly, whereas chronic pain increases the basal and noxious stimulus-induced firing rates in the ACC, it has the opposite effect on the PL-PFC 30 . Thus, a reduction in PFC activities and an enhancement in ACC activities may play potentially complementary roles in the chronic pain state.…”

Section: Discussionmentioning

confidence: 95%

“…For neuronal spike analysis, we calculated PSTHs using a 5 s range before and after peripheral stimulus 30 . The number of spikes in each stimulus-aligned bin was averaged across all trials to create the PSTH.…”

Section: Methodsmentioning

confidence: 99%

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Ketamine reduces aversion in rodent pain models by suppressing hyperactivity of the anterior cingulate cortex

et al. 2018

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Chronic pain is known to induce an amplified aversive reaction to peripheral nociceptive inputs. This enhanced affective response constitutes a key pathologic feature of chronic pain syndromes such as fibromyalgia. However, the neural mechanisms that underlie this important aspect of pain processing remain poorly understood, hindering the development of treatments. Here, we show that a single dose of ketamine can produce a persistent reduction in the aversive response to noxious stimuli in rodent chronic pain models, long after the termination of its anti-nociceptive effects. Furthermore, we demonstrated that this anti-aversive property is mediated by prolonged suppression of the hyperactivity of neurons in the anterior cingulate cortex (ACC), a brain region well known to regulate pain affect. Therefore, our results indicate that it is feasible to dissociate the affective from the sensory component of pain, and demonstrate the potential for low-dose ketamine to be an important therapy for chronic pain syndromes.

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Section: Resultssupporting

confidence: 91%

Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 95%

Section: Methodsmentioning

confidence: 99%

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Ketamine reduces aversion in rodent pain models by suppressing hyperactivity of the anterior cingulate cortex

et al. 2018

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“…Two video cameras (120 frame per second) were used to continuously monitor the rat’s behavior during the course of experiment. Details are referred to previous publications [7, 25].…”

Section: Methodsmentioning

confidence: 99%

Predictive coding models for pain perception

Song

Yao

Kemprecos

et al. 2019

Preprint

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Pain is a complex, multidimensional experience that involves dynamic interactions between sensory-discriminative and affective-emotional processes. Pain experiences have a high degree of variability depending on their context and prior anticipation. Viewing pain perception as a perceptual inference problem, we use a predictive coding paradigm to characterize both evoked and spontaneous pain. We record the local field potentials (LFPs) from the primary somatosensory cortex (S1) and the anterior cingulate cortex (ACC) of freely behaving rats-two regions known to encode the sensory-discriminative and affective-emotional aspects of pain, respectively. We further propose a framework of predictive coding to investigate the temporal coordination of oscillatory activity between the S1 and ACC. Specifically, we develop a high-level, empirical and phenomenological model to describe the macroscopic dynamics of bottom-up and top-down activity. Supported by recent experimental data, we also develop a mechanistic mean-field model to describe the mesoscopic population neuronal dynamics in the S1 and ACC populations, in both naive and chronic pain-treated animals. Our proposed predictive coding models not only replicate important experimental findings, but also provide new mechanistic insight into the uncertainty of expectation, placebo or nocebo effect, and chronic pain. Author SummaryPain perception in the mammalian brain is encoded through multiple brain circuits.The experience of pain is often associated with brain rhythms or neuronal oscillations at different frequencies. Understanding the temporal coordination of neural oscillatory activity from different brain regions is important for dissecting pain circuit mechanisms and revealing differences between distinct pain conditions. Predictive coding is a general computational framework to understand perceptual inference by integrating bottom-up sensory information and top-down expectation. Supported by experimental data, we propose a predictive coding framework for pain perception, and develop empirical and biologically-constrained computational models to characterize oscillatory dynamics of neuronal populations from two cortical circuits-one for the sensory-discriminative PLOS 2/49 experience and the other for affective-emotional experience, and further characterize their temporal coordination under various pain conditions. Our computational study of biologically-constrained neuronal population model reveals important mechanistic insight on pain perception, placebo analgesia, and chronic pain. Introduction 1Pain is a basic experience that is subjective and multidimensional. Pain processing 2 involves sensory, affective, and cognitive processing across distributed neural 3 circuits [1-5]. However, a complete understanding of pain perception and cortical pain 4 processing has remained elusive. Given the same nociceptive stimuli, the context 5 matters for pain percept. Human neuroimaging studies have shown that among many 6 brain regions, the primary somatosensory cortex (S1) a...

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Reattribution to Mind-Brain Processes and Recovery From Chronic Back Pain

Ashar,

Lumley,

Perlis

et al. 2023

JAMA Netw Open

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ImportanceIn primary chronic back pain (CBP), the belief that pain indicates tissue damage is both inaccurate and unhelpful. Reattributing pain to mind or brain processes may support recovery.ObjectivesTo test whether the reattribution of pain to mind or brain processes was associated with pain relief in pain reprocessing therapy (PRT) and to validate natural language–based tools for measuring patients’ symptom attributions.Design, Setting, and ParticipantsThis secondary analysis of clinical trial data analyzed natural language data from patients with primary CBP randomized to PRT, placebo injection control, or usual care control groups and treated in a US university research setting. Eligible participants were adults aged 21 to 70 years with CBP recruited from the community. Enrollment extended from 2017 to 2018, with the current analyses conducted from 2020 to 2022.InterventionsPRT included cognitive, behavioral, and somatic techniques to support reattributing pain to nondangerous, reversible mind or brain causes. Subcutaneous placebo injection and usual care were hypothesized not to affect pain attributions.Main Outcomes and MeasuresAt pretreatment and posttreatment, participants listed their top 3 perceived causes of pain in their own words (eg, football injury, bad posture, stress); pain intensity was measured as last-week average pain (0 to 10 rating, with 0 indicating no pain and 10 indicating greatest pain). The number of attributions categorized by masked coders as reflecting mind or brain processes were summed to yield mind-brain attribution scores (range, 0-3). An automated scoring algorithm was developed and benchmarked against human coder–derived scores. A data-driven natural language processing (NLP) algorithm identified the dimensional structure of pain attributions.ResultsWe enrolled 151 adults (81 female [54%], 134 White [89%], mean [SD] age, 41.1 [15.6] years) reporting moderate severity CBP (mean [SD] intensity, 4.10 [1.26]; mean [SD] duration, 10.0 [8.9] years). At pretreatment, 41 attributions (10%) were categorized as mind- or brain-related across intervention conditions. PRT led to significant increases in mind- or brain-related attributions, with 71 posttreatment attributions (51%) in the PRT condition categorized as mind- or brain-related, as compared with 22 (8%) in control conditions (mind-brain attribution scores: PRT vs placebo, g = 1.95 [95% CI, 1.45-2.47]; PRT vs usual care, g = 2.06 [95% CI, 1.57-2.60]). Consistent with hypothesized PRT mechanisms, increases in mind-brain attribution score were associated with reductions in pain intensity at posttreatment (standardized β = −0.25; t127 = −2.06; P = .04) and mediated the effects of PRT vs control on 1-year follow-up pain intensity (β = −0.35 [95% CI, −0.07 to −0.63]; P = .05). The automated word-counting algorithm and human coder-derived scores achieved moderate and substantial agreement at pretreatment and posttreatment (Cohen κ = 0.42 and 0.68, respectively). The data-driven NLP algorithm identified a principal dimension of mind and brain vs biomechanical attributions, converging with hypothesis-driven analyses.Conclusions and RelevanceIn this secondary analysis of a randomized trial, PRT increased attribution of primary CBP to mind- or brain-related causes. Increased mind-brain attribution was associated with reductions in pain intensity.

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Scaling Up Cortical Control Inhibits Pain

Cited by 70 publications

References 39 publications

Ketamine reduces aversion in rodent pain models by suppressing hyperactivity of the anterior cingulate cortex

Ketamine reduces aversion in rodent pain models by suppressing hyperactivity of the anterior cingulate cortex

Predictive coding models for pain perception

Reattribution to Mind-Brain Processes and Recovery From Chronic Back Pain

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