Common cortical network for first and second pain

Forss, Nina; Raij, Tuukka T.; Seppä, Mika; Hari, Riitta

doi:10.1016/j.neuroimage.2004.09.032

Cited by 80 publications

(57 citation statements)

References 82 publications

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“…According to our EEG-informed BOLD analyses, activation of the pain matrix starts with contralateral S2 in the time window 140-160ms poststimulus which is also consistent with previous EEG-, MEG, and intracortical findings [Forss et al, 2005;Frot et al, 2008;Garcia-Larrea et al, 2003, Ohara et al, 2004aPloner et al, 2002]. When scalp-recorded event-related EEG potentials in response to laser stimulation (LEPs) are used to study the temporal dynamics of pain processing, the first detectable LEP is the N1 component that is often reported to peak 140-160 ms poststimulus for hand stimulation [Garcia-Larrea et al, 2003 and references therein].…”

Section: Discussionsupporting

confidence: 89%

Dynamic EEG‐informed fMRI modeling of the pain matrix using 20‐ms root mean square segments

Brinkmeyer¹,

Mobascher²,

Warbrick³

et al. 2010

Human Brain Mapping

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Previous studies on the spatio-temporal dynamics of cortical pain processing using electroencephalography (EEG), magnetoencephalography (MEG), or intracranial recordings point towards a high degree of parallelism, e.g. parallel instead of sequential activation of primary and secondary somatosensory areas or simultaneous activation of somatosensory areas and the mid-cingulate cortex. However, because of the inverse problem, EEG and MEG provide only limited spatial resolution and certainty about the generators of cortical pain-induced electromagnetic activity, especially when multiple sources are simultaneously active. On the other hand, intracranial recordings are invasive and do not provide whole-brain coverage. In this study, we thought to investigate the spatio-temporal dynamics of cortical pain processing in 10 healthy subjects using simultaneous EEG/functional magnetic resonance imaging (fMRI). Voltages of 20 ms segments of the EEG root mean square (a global, largely reference-free measure of event-related EEG activity) in a time window 0-400 ms poststimulus were used to model trial-to-trial fluctuations in the fMRI blood oxygen level dependent (BOLD) signal. EEG-derived regressors explained additional variance in the BOLD signal from 140 ms poststimulus onward. According to this analysis, the contralateral parietal operculum was the first cortical area to become activated upon painful laser stimulation. The activation pattern in BOLD analyses informed by subsequent EEG-time windows suggests largely parallel signal processing in the bilateral operculo-insular and mid-cingulate cortices. In that regard, our data are in line with previous reports. However, the approach presented here is noninvasive and bypasses the inverse problem using only temporal information from the EEG.

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Section: Discussionsupporting

confidence: 89%

Dynamic EEG‐informed fMRI modeling of the pain matrix using 20‐ms root mean square segments

Brinkmeyer¹,

Mobascher²,

Warbrick³

et al. 2010

Human Brain Mapping

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“…For example, when the same laser-heat pain stimulus was used in both fMRI and MEG settings, the AI activation was evident in the fMRI measurements , but the MEG responses of the lateral cortex were adequately explained by activation of the second somatosensory cortex [Forss et al, 2005]. Indeed, according to our simulation using the anatomy of one subject, the source current in AI should be three to four times stronger than that in STS to produce an MEG response of the same magnitude.…”

Section: Differences Between Neuromagnetic and Hemodynamic Responses mentioning

confidence: 81%

Facial expressions of pain modulate observer's long‐latency responses in superior temporal sulcus

Kujala¹,

Tanskanen²,

Parkkonen³

et al. 2009

Human Brain Mapping

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The strength of brain responses to others' pain has been shown to depend on the intensity of the observed pain. To investigate the temporal profile of such modulation, we recorded neuromagnetic brain responses of healthy subjects to facial expressions of pain. The subjects observed grayscale photos of the faces of genuine chronic pain patients when the patients were suffering from their ordinary pain (Chronic) and when the patients' pain was transiently intensified (Provoked). The cortical activation sequence during observation of the facial expressions of pain advanced from occipital to temporo-occipital areas, and it differed between Provoked and Chronic pain expressions in the right middle superior temporal sulcus (STS) at 300-500 ms: the responses were about a third stronger for Provoked than Chronic pain faces. Furthermore, the responses to Provoked pain faces were about 40% stronger in the right than the left STS, and they decreased from the first to the second measurement session by one-fourth, whereas no similar decrease in responses was found for Chronic pain faces. Thus, the STS responses to the pain expressions were modulated by the intensity of the observed pain and by stimulus repetition; the location and latency of the responses suggest close similarities between processing of pain and other affective facial expressions.

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“…For example, in SI and thalamus, but not in SII, activation has been recorded in response to painful stimulation, although the level of activation was significantly greater in the hemisphere contralateral to the stimulus [58] , whereas selective activation of nociceptive nerve fibers Adelta and C by thulium-laser stimulation of skin evoked cortical responses in SII but not SI [59] . Further studies show that abnormal pain evoked by innocuous stimuli (allodynia) is associated with amplification of the thalamic, insular and SII responses, but not SI responses [60] , and that no painful sensation was evoked in the SI of 14 patients referred for epilepsy surgery [61] .…”

Section: Involvement Of Si and Sii In Nociception Modulationmentioning

confidence: 95%

Cerebral cortex modulation of pain

2008

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Pain is a complex experience encompassing sensory-discriminative, affective-motivational and cognitiv e-emotional components mediated by different mechanisms. Contrary to the traditional view that the cerebral cortex is not involved in pain perception, an extensive cortical network associated with pain processing has been revealed using multiple methods over the past decades. This network consistently includes, at least, the anterior cingulate cortex, the agranular insular cortex, the primary (SΙ) and secondary somatosensory (SΠ) cortices, the ventrolateral orbital cortex and the motor cortex. These cortical structures constitute the medial and lateral pain systems, the nucleus submedius-ventrolateral orbital cortex-periaqueductal gray system and motor cortex system, respectively. Multiple neurotransmitters, including opioid, glutamate, GABA and dopamine, are involved in the modulation of pain by these cortical structures. In addition, glial cells may also be involved in cortical modulation of pain and serve as one target for pain management research. This review discusses recent studies of pain modulation by these cerebral cortical structures in animals and human.

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Common cortical network for first and second pain

Cited by 80 publications

References 82 publications

Dynamic EEG‐informed fMRI modeling of the pain matrix using 20‐ms root mean square segments

Dynamic EEG‐informed fMRI modeling of the pain matrix using 20‐ms root mean square segments

Facial expressions of pain modulate observer's long‐latency responses in superior temporal sulcus

Cerebral cortex modulation of pain

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