Neural indicators of perceptual variability of pain across species

Hu, Li; Iannetti, Gian Domenico

doi:10.1073/pnas.1812499116

Cited by 143 publications

(165 citation statements)

References 48 publications

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“…Third, it is still unclear whether pain sensitivity varies with the development of the disease (i.e., acute, remission, chronic). To address this issue, our findings ought to be tested in prodromal‐phase or first‐episode patients in a longitudinal study, especially considering the tremendous differences of pain sensitivity across individuals (Hu & Iannetti, ). Forth, we did not detect the relationship between clinical symptoms (illness severity, positive or negative symptom, and cognitive impairments, etc.)…”

Section: Discussionmentioning

confidence: 99%

A modality‐specific dysfunction of pain processing in schizophrenia

Zhou

Liang

et al. 2019

Human Brain Mapping

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Clinical observations showed that schizophrenia (SCZ) patients reported little or no pain under various conditions that are commonly associated with intense painful sensations, leading to a higher risk of morbidity and mortality. However, this phenomenon has received little attention and its underlying neural mechanisms remain unclear. Here, we conducted two experiments combining psychophysics, electroencephalography (EEG), and functional magnetic resonance imaging (fMRI) techniques to investigate neural mechanisms of pain insensitivity in SCZ patients. Specifically, we adopted a stimulus–response paradigm with brief stimuli of different sensory modalities (i.e., nociceptive, non‐nociceptive somatosensory, and auditory) to test whether pain insensitivity in SCZ patients is supra‐modal or modality‐specific, and used EEG and fMRI techniques to clarify its neural mechanisms. We observed that perceived intensities to nociceptive stimuli were significantly smaller in SCZ patients than healthy controls, whereas perceived intensities to non‐nociceptive somatosensory and auditory stimuli were not significantly different. The behavioral results were confirmed by stimulus‐evoked brain responses sampled by EEG and fMRI techniques, thus verifying the modality‐specific nature of the modulation of nociceptive information processing in SCZ patients. Additionally, significant group differences were observed in the spectral power of alpha oscillations in prestimulus EEG and the seed‐based functional connectivity in resting‐state fMRI (seeds: the thalamus and periaqueductal gray that are key nodes in ascending and descending pain pathways respectively), suggesting a possible contribution of cortical–subcortical dysfunction to the phenomenon. Overall, our study provides insight into the neural mechanisms of pain insensitivity in SCZ and highlights a need for systematic assessments of their pain‐related diseases.

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Section: Discussionmentioning

confidence: 99%

A modality‐specific dysfunction of pain processing in schizophrenia

Zhou

Liang

et al. 2019

Human Brain Mapping

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“…In subjects who rated the nociceptive stimulus as more painful the phase of neural activity at 0.1 Hz was closer to that of the stimulus input. This is an important finding given that almost all nociceptive-evoked neural responses fail to track pain sensitivity across subjects, in both human and animal studies (42).…”

Section: Resultsmentioning

confidence: 97%

“…expectation, stimulus repetition, presentation of non-painful but iso-salient stimuli, congenital insensitivity to pain; (60–62)). Second, almost all nociceptive-evoked neural responses fail to track pain sensitivity across subjects , in both human and animal studies (42).…”

Section: Discussionmentioning

confidence: 99%

“…Relevant to this discourse, a recent study revealed that brain oscillations in the gamma band index the variability of pain sensitivity across individuals, in both humans and rodents (42). However, the clinical relevance of this observation is limited because (i) gamma oscillations were elicited by transient nociceptive stimuli causing painful sensations barely reflecting clinical pain, and (ii) due to low signal-to-noise ratio, gamma oscillations are hardly detected in EEG recordings from single individuals.…”

Section: Discussionmentioning

confidence: 99%

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Ultra-low frequency neural entrainment to pain

Guo

Bufacchi

Novembre

et al. 2019

Preprint

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30Nervous systems exploit regularities in the sensory environment to predict sensory input and adjust 31 behavior, and thereby maximize fitness. Entrainment of neural oscillations allows retaining temporal 32 regularities of sensory information, a prerequisite for prediction. Entrainment has been extensively 33 described at the frequencies of periodic inputs most commonly present in visual and auditory landscapes 34 (e.g. >1 Hz). An open question is whether neural entrainment also occurs for regularities at much longer 35timescales. Here we exploited the fact that the temporal dynamics of thermal stimuli in natural environment 36can unfold very slowly. We show that ultra-low frequency neural oscillations preserved a long-lasting trace 37 of sensory information through neural entrainment to periodic thermo-nociceptive input as low as 0.1 Hz. 38Importantly, revealing the functional significance of this phenomenon, both power and phase of the 39 entrainment predicted individual pain sensitivity. In contrast, periodic auditory input at the same ultra-low 40 frequency did not entrain ultra-low frequency oscillations. These results demonstrate that a functionally-41 significant neural entrainment can occur at temporal scales far longer than those commonly explored. The 42 non-supramodal nature of our results suggests that ultra-low frequency entrainment might be tuned to the 43 temporal scale of the statistical regularities characteristic of different sensory modalities. 44

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“…We conducted five experiments on 130 healthy human subjects in total. High-power laser stimulation was applied to selectively excite cutaneous nociceptors and thereby elicit pure painful percepts without tactile sensations (25,26). For all experiments, the energy of laser stimuli was individually determined by increasing stimulus energy in steps of 0.25 J, until a rating of 7 was obtained on a numerical rating scale ranging from 0 (no pain) to 10 (the worst pain imaginable).…”

Section: Resultsmentioning

confidence: 99%

Three distinct neural mechanisms support movement-induced analgesia

Yao

Thompson³

et al. 2020

Preprint

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Pain is essential for our survival by protecting us from severe injuries. Pain signals may be exacerbated by continued physical activities but can also be interrupted or over-ridden by physical movements, a process called movement-induced analgesia. A number of neural mechanisms have been proposed to account for this effect, including the reafference principle, the gate control theory of pain, and the top-down psychological modulation. Given that the analgesic effects of these mechanisms are temporally overlapping, it is unclear whether movement-induced analgesia results from a single neural mechanism or the joint action of multiple neural mechanisms. To address this question, we conducted five experiments on 130 healthy human subjects. First, the frequency of hand shaking was manipulated in order to quantify the relationship between the strength of the voluntary movement and the analgesic effect. Second, the temporal delay (between hand shaking and nociceptive laser stimuli) and the stimulated side (nociceptive laser stimuli were delivered on the hand ipsilateral or contralateral to the shaken one) were manipulated to quantify the temporal and spatial characteristics of the analgesic effect induced by voluntary movement. Combining psychophysics and electroencephalographic recordings, we demonstrated that movement-induced analgesia is a result of the joint action of multiple neural mechanisms. This investigation is the first to disentangle the distinct contributions of different neural mechanisms to the analgesic effect of voluntary movement. These findings extend our understanding of sensory attenuation arising from voluntary movement and may prove instrumental in the development of new strategies in pain management.

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Neural indicators of perceptual variability of pain across species

Cited by 143 publications

References 48 publications

A modality‐specific dysfunction of pain processing in schizophrenia

A modality‐specific dysfunction of pain processing in schizophrenia

Ultra-low frequency neural entrainment to pain

Three distinct neural mechanisms support movement-induced analgesia

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