Temporal changes in cortical activation during distraction from pain: A comparative LORETA study with conditioned pain modulation

Moont, Ruth; Crispel, Yonatan; Lev, Rina; Pud, Dorit; Yarnitsky, David

doi:10.1016/j.brainres.2011.11.056

Cited by 45 publications

(41 citation statements)

References 70 publications

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“…The increased activity in the anterior INS and DLPFC during the OA induction of analgesia is in line with previous studies that found involvement of these regions in analgesia using placebo, meditation and distraction [14,44,35,22,10]. Given that OA activation of the anterior INS and DLPFC mirrors the activity of brain regions engaged in the modulation of pain by cognitive processes, this finding raises the possibility that portion of OA is mediated or amplified by cognitive processes related to the prediction of the time course of pain.…”

Section: Discussionsupporting

confidence: 91%

Distinct brain mechanisms support spatial vs temporal filtering of nociceptive information

Nahman‐Averbuch

Martucci

Granovsky

et al. 2014

Pain

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100

117

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The role of endogenous analgesic mechanisms has largely been viewed in the context of gain modulation during nociceptive processing. However, these analgesic mechanisms may play critical roles in the extraction and subsequent utilization of information related to spatial and temporal features of nociceptive input. To date, it remains unknown if spatial and temporal filtering of nociceptive information is supported by similar analgesic mechanisms. To address this question, human volunteers were recruited to assess brain activation with functional MRI during conditioned pain modulation (CPM) and offset analgesia (OA). CPM provides one paradigm for assessing spatial filtering of nociceptive information while OA provides a paradigm for assessing temporal filtering of nociceptive information. CPM and OA both produced statistically significant reductions in pain intensity. However, the magnitude of pain reduction elicited by CPM was not correlated with that elicited by OA across different individuals. Different patterns of brain activation were consistent with the psychophysical findings. CPM elicited widespread reductions in regions engaged in nociceptive processing such as the thalamus, insula and SII. OA produced reduced activity in SI, but was associated with greater activation in the anterior insula, dorso-lateral prefrontal cortex, intra-parietal sulcus, and inferior parietal lobule relative to CPM. In the brainstem, CPM consistently produced reductions in activity while OA produced increases in activity. Conjunction analysis confirmed that CPM related activity did not overlap with that of OA. Thus, dissociable mechanisms support inhibitory processes engaged during spatial vs. temporal filtering of nociceptive information.

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Section: Discussionsupporting

confidence: 91%

Distinct brain mechanisms support spatial vs temporal filtering of nociceptive information

Nahman‐Averbuch

Martucci

Granovsky

et al. 2014

Pain

Self Cite

100

117

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“…Using animal studies, these authors demonstrated that pain occurring in one part of the body reduces pain in the rest of the body by activating these DNIC, which are spinal and supra-spinal (i.e., subnucleus reticularis dorsalis in the brainstem) neural mechanisms that modulate the transmission of nociceptive signals via multi-receptive neurons . DNIC-like mechanisms have also repeatedly been observed in humans, where the application of a tonic pain stimulus has been shown to reduce the sensitivity for a concurrently applied phasic pain stimulus (going along with an increase in pain inhibitory frontal areas before decreasing in primary somatosensory areas (Piche et al 2009;Moont et al 2012)). A consensus group decided to use a different terminology for such tests in humans, by calling them CPM and thus, separating them from DNIC, which had been defined in pure physiological terms (Yarnitsky et al 2010).…”

Section: Introductionmentioning

confidence: 94%

Chemo-somatosensory evoked potentials: A sensitive tool to assess conditioned pain modulation?

Kunz

Mohammadian

Renner

et al. 2014

Somatosensory & Motor Research

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The experimental pain model using CO₂ stimuli to elicit CSSEPs proved to be sensitive enough to capture weak CPM effects elicited by a conditioning stimulus of rather low noxious load. The usage of such mild noxious conditioning stimuli-in contrast to stimuli of higher noxious load (e.g., cold pressor test)-has the advantage that the activation of other types of pain inhibitory mechanisms in parallel (like attentional distraction, stress-induced analgesia) can be avoided.

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“…The neural substrates of pain perception have been intensively explored with neuroimaging techniques, such as fMRI and positron emission tomography (Hanakawa, 2012). Many imaging studies have consistently revealed a set of brain regions as substrates of pain perception (Moisset & Bouhassira, 2007;Moont, Crispel, Lev, Pud, & Yarnitsky, 2012). These regions include the anterior cingulate cortex, the insula, the parietal operculum including the second somatosensory cortex, and the thalamus, which are collectively called the pain matrix.…”

Section: Introductionmentioning

confidence: 99%

Pain Management Using 19-ElectrodeZ-Score LORETA Neurofeedback

Koberda¹,

Koberda²,

Bienkiewicz³

et al. 2013

Journal of Neurotherapy

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Temporal changes in cortical activation during distraction from pain: A comparative LORETA study with conditioned pain modulation

Cited by 45 publications

References 70 publications

Distinct brain mechanisms support spatial vs temporal filtering of nociceptive information

Distinct brain mechanisms support spatial vs temporal filtering of nociceptive information

Chemo-somatosensory evoked potentials: A sensitive tool to assess conditioned pain modulation?

Pain Management Using 19-ElectrodeZ-Score LORETA Neurofeedback

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