Pain experience includes the fine-grain integration of both attentive and automatic (bottom-up; Legrain et al., 2012), as well as affective and intentional (top-down; Buschman and Miller, 2007) processes. While the neural underpinnings of post-stimulus pain processing have been deeply explored (Hauck et al., 2008), the oscillatory brain activity preceding pain processing is less far investigated

Nicolardi, Valentina

Spinelli, Giuseppe

English

PubMed

Giuseppe Spinelli

Valentina Nicolardi

Frontiers - Publisher Connector

Commentary: Prestimulus Theta Oscillations and Connectivity Modulate Pain Perception

GENERAL COMMENTARY
published: 26 October 2016
doi: 10.3389/fnhum.2016.00535
Frontiers in Human Neuroscience | www.frontiersin.org 1 October 2016 | Volume 10 | Article 535
Edited by:
Vladimir Litvak,
UCL Institute of Neurology, UK
Reviewed by:
Michael X. Cohen,
University of Amsterdam, Netherlands
*Correspondence:
Giuseppe Spinelli
giuseppe.spinelli@uniroma1.it
Valentina Nicolardi
valentina.nicolardi@uniroma1.it
†
These authors have contributed
equally to this work.
Received: 10 September 2016
Accepted: 10 October 2016
Published: 26 October 2016
Citation:
Spinelli G and Nicolardi V (2016)
Commentary: Prestimulus Theta
Oscillations and Connectivity
Modulate Pain Perception.
Front. Hum. Neurosci. 10:535.
doi: 10.3389/fnhum.2016.00535
Commentary: Prestimulus Theta
Oscillations and Connectivity
Modulate Pain Perception
Giuseppe Spinelli 1, 2*† and Valentina Nicolardi 1, 2*†
1Department of Psychology, Sapienza University of Rome, Rome, Italy, 2 IRCCS Santa Lucia Foundation, Rome, Italy
Keywords: feedback processing, gamma oscillations, pain perception, salience processing, theta oscillations
A commentary on
Prestimulus Theta Oscillations and Connectivity Modulate Pain Perception
by Taesler, P., and Rose, M., (2016). J. Neurosci. 36, 5026–5033. doi: 10.1523/JNEUROSCI.3325-
15.2016
Pain experience includes the fine-grain integration of both attentive and automatic (bottom-up;
Legrain et al., 2012), as well as affective and intentional (top-down; Buschman and Miller, 2007)
processes. While the neural underpinnings of post-stimulus pain processing have been deeply
explored (Hauck et al., 2008), the oscillatory brain activity preceding pain processing is less far
investigated.
In a recent issue of Journal of Neuroscience, Taesler and Rose (2016) addresses this topic by
recording EEG from healthy participants who were forced to judge as “painful” or “non-painful”
series of electrical stimulations delivered on their own left-hand. Painful stimulation was elegantly
kept constant at the painful-threshold of each participant, and a subtractive approach (“painful”
minus “non-painful” trials) was adopted to study the EEG signatures underlying pain processing.
Results revealed enhanced pre-stimulus theta and gamma activity. Specifically, pre-stimulus
theta power was both increased and decreased over fronto-temporal ipsilateral and contralateral
electrodes, respectively. Instead, pre-stimulus gamma power was enhanced over frontal and
temporal electrodes. Tellingly, while the ipsilateral reduction of theta-band power paralleled a
decreased theta-band connectivity over frontal-lateral electrodes, the contralateral increase resulted
in an enhanced connectivity of a bilateral fronto-temporal/centro-parietal network. Also, the
connectivity-pattern of the gamma increased between Fz and a parieto-temporal cluster around P6.
Interestingly, source-analysis revealed likely generators in the bilateral insular cortex and posterior
cingulate cortex for the theta, and contralateral insular cortex for the gamma band.
While this paper provides interesting and novel findings, we believe that these results deserve
to be further discussed and interpreted in view of (i) the state-of-art literature of pain, and (ii)
an integrated neurocognitive model of that takes into account both pain and negative-feedback
processing.
First, the core of discussion of the authors aims at interpreting pre-stimulus theta oscillations as
the vehicle by which both contra- and ipsi-lateral insular cortices communicate to process painful
stimulation. This relevant result is compared to two previous studies (Sarnthein et al., 2006;Walton
et al., 2010) on chronic-pain patients, in which, however, only post-stimulus theta oscillations were
related to pain processing. Thus, while Taesler and Rose provided relevant additions to the literature
on pain processing, a direct comparison with these latter studies is still difficult to be assessed
given the different neurocognitive mechanisms underlying the processing of pain in individuals
with chronic sensitization respect to healthies (Bushnell et al., 2013).
Spinelli and Nicolardi Prestimulus Theta Modulate Pain Perception
Moreover, the pre-stimulus theta-band power increase can
be viewed from a different perspective when considering that
the paradigm of Taesler and Rose, by delivering in each trial
a constant painful stimulation after a fixation-cross, induces
a strong “stimulus–stimulus” association. This trial-by-trial
“stimulus–stimulus” reinforcement, can induce an expectancy of
pain thatmight lead the neurocognitive system of pain processing
to be active before the onset of the actual painful stimulation.
Such an affective and anticipatory activation is in keeping with
previous evidences (Palermo et al., 2015; Sawamoto et al., 2000)
showing that expectation of pain amplifies brain responses to
the somatosensory stimulation and activates mainly the anterior
cingulate cortex and insular cortices.
Consequently, given that both insular cortices and various
regions of the middle-frontal cortex (Ridderinkhof et al.,
2004), are linked to pre- and post-conflict monitoring (Yeung
et al., 2004), feedback-monitoring and reinforcement-learning
(Holroyd and Coles, 2002) via increasing theta band oscillations
(Cohen, 2014), we argue that the pain processing system can
share the same temporal dynamics as the performance (and
conflict) monitoring system (Shackman et al., 2011). In fact,
it is worth noting how in Taesler and Rose the displacement
of theta oscillations from pre- to post-stimulus, evolves
from insular cortices to fronto-central and dorso-lateral
ones. In this view, we suggest that the temporal dynamics
of processing painful stimulation can develop from an early
affective, orienting/salience response to unpleasant/unfavorable
outcomes—processed by right and left insular cortices
prior to painful stimulation—to a late processing of the
unfavorable/painful outcome itself—processed by frontal
regions after painful stimulation. Accordingly, the theta-related
connectivity pattern showed by Taesler and Rose, seems to
resemble the pattern of activation usually found when the
so-called “saliency network”—mostly governed by the anterior
insular cortex—attempt to elicit a (re)orienting response
before negative outcomes. In fact, it is arguably known how
the activation of the anterior insular activity, by signaling an
increased likelihood to receive unfavorable outcomes, aims at
rapidly calling for additional cognitive control or behavioral
adjustment (Klein et al., 2007). Thus, considering that in Taesler
and Rose, participants were always stimulated at their own
painful threshold, the activity in the insular cortices could
have governed, via theta increase, two different processes,
namely: (i) the integration of personally/motivationally
information linked to painful stimulation and (ii) the
preparatory allocation of cognitive and physical resources
of salience processing. While the latter is in keeping with
previous evidence (Sridharan et al., 2008), the former can be
addressed to the notion that pain-related cortical responses
reflect the processing of saliency of painful stimulations that
is related to a salience-specific multimodal neural activity
rather than pain-specific unimodal neural response (Valentini
et al., 2011). However, studies investigating this latter issue in
the pre-stimulus interval are still missing, and further effort
is needed to explore the link between these two cognitive
processes and the underlying electro-cortical signatures of pain
processing.
Contrarily, the later stage of pain detection and the post-
stimulus theta synchronization over middle-frontal and parieto-
occipital brain regions, has been less discussed by the authors.
It is worth mentioning that the pre-stimulus theta activation
over the bi-lateral insular cortices shifts over fronto-central
scalp location during the post-stimulus processing. Interestingly,
such an increase over mid-frontal electrodes might be linked
to the neurophysiological coding of: (i) individual psychological
traits during processing of painful stimuli (Schulz et al., 2012),
and (ii) negative outcome monitoring related to a recruitment
of top-down cognitive processes to ultimately adapt future
behavior. This latter hypothesis needs to be tested as it
could represent a valid integration of the saliency-processing
theory (Iannetti and Mouraux, 2010) and the performance-
monitoring model. In this view, painful stimulation might
be processed by the brain in the same way as negative
feedback/outcome (Shackman et al., 2011), and its detection
and encoding may be reflected in a coupling between
post-stimulus theta-gamma oscillations, where theta might
be considered an high-level/ cognitive cortical marker of
mismatch detection, and the gamma a low-level/perceptual
neural signature of the saliency and the intensity of pain
processing, respectively.
Concluding, Taesler and Rose provided optimal evidences to
deepen the functional significance of theta oscillations evoked
before and after painful stimulation. Based on our arguments
we also believe that future investigations should focus on an
integrative neuro-cognitive model of pain perception that should
take into account also negative/unpleasant outcome monitoring,
performance monitoring models, and their underlying electro-
cortical signatures.
AUTHOR CONTRIBUTIONS
GS and VN equally contributed to read, comment, and write the
commentary.
ACKNOWLEDGMENTS
The authors are grateful to Prof. Salvatore Maria Aglioti for his
comments.
REFERENCES
Buschman, T. J., and Miller, E. K. (2007). Top-down versus bottom-up control
of attention in the prefrontal and posterior parietal cortices. Science 315,
1860–1862. doi: 10.1126/science.1138071
Bushnell, M. C., Ceko, M., and Low, L. A. (2013). Cognitive and emotional control
of pain and its disruption in chronic pain. Nat. Rev. Neurosci. 14, 502–511. doi:
10.1038/nrn3516
Cohen, M. X. (2014). A neural microcircuit for cognitive conflict detection and
signaling. Trends Neurosci. 37, 480–490. doi: 10.1016/j.tins.2014.06.004
Frontiers in Human Neuroscience | www.frontiersin.org 2 October 2016 | Volume 10 | Article 535
Spinelli and Nicolardi Prestimulus Theta Modulate Pain Perception
Hauck, M., Lorenz, J., and Engel, A. K. (2008). Role of synchronized oscillatory
brain activity for human pain perception. Rev. Neurosci. 19, 441–450. doi:
10.1515/REVNEURO.2008.19.6.441
Holroyd, C. B., and Coles, M. G. (2002). The neural basis of human error
processing: reinforcement learning, dopamine, and the error-related negativity.
Psychol. Rev. 109, 679. doi: 10.1037/0033-295x.109.4.679
Iannetti, G. D., and Mouraux, A. (2010). From the neuromatrix to the pain
matrix (and back). Exp. Brain Res. 205, 1–12. doi: 10.1007/s00221-010-2
340-1
Klein, T. A., Endrass, T., Kathmann, N., Neumann, J., von Cramon, D. Y., and
Ullsperger, M. (2007). Neural correlates of error awareness. Neuroimage 34,
1774–1781. doi: 10.1016/j.neuroimage.2006.11.014
Legrain, V., Mancini, F., Sambo, C. F., Torta, D. M., Ronga, I., and
Valentini, E. (2012). Cognitive aspects of nociception and pain: bridging
neurophysiology with cognitive psychology. Neurophysiol. Clin. 42, 325–336.
doi: 10.1016/j.neucli.2012.06.003
Palermo, S., Benedetti, F., Costa, T., and Amanzio, M. (2015). Pain anticipation: an
activation likelihood estimation meta-analysis of brain imaging studies. Hum.
Brain Mapp. 36, 1648–1661. doi: 10.1002/hbm.22727
Ridderinkhof, K. R., Ullsperger, M., Crone, E. A., and Nieuwenhuis, S. (2004). The
role of the medial frontal cortex in cognitive control. Science 306, 443–447. doi:
10.1126/science.1100301
Sarnthein, J., Stern, J., Aufenberg, C., Rousson, V., and Jeanmonod, D.
(2006). Increased EEG power and slowed dominant frequency in
patients with neurogenic pain. Brain 129, 55–64. doi: 10.1093/brain/a
wh631
Sawamoto, N., Honda, M., Okada, T., Hanakawa, T., Kanda, M., Fukuyama,
H., et al. (2000). Expectation of pain enhances responses to nonpainful
somatosensory stimulation in the anterior cingulate cortex and parietal
operculum/posterior insula: an event-related functional magnetic resonance
imaging study. J. Neurosci. 20, 7438–7445. doi: 10.11501/3183115
Shackman, A. J., Salomons, T. V., Slagter, H. A., Fox, A. S., Winter, J. J.,
and Davidson, R. J. (2011). The integration of negative affect, pain and
cognitive control in the cingulate cortex. Nat. Rev. Neurosci. 12, 154–167. doi:
10.1038/nrn2994
Sridharan, D., Levitin, D. J., and Menon, V. (2008). A critical role for
the right fronto-insular cortex in switching between central-executive and
default-mode networks. Proc. Natl. Acad. Sci. U.S.A. 105, 12569–12574. doi:
10.1073/pnas.0800005105
Schulz, E., Tiemann, L., Witkovsky, V., Schmidt, P., and Ploner, M. (2012).
γ Oscillations are involved in the sensorimotor transformation of pain. J.
Neurophysiol. 108, 1025–1031. doi: 10.1152/jn.00186.2012
Taesler, P., and Rose, M. (2016). Prestimulus Theta Oscillations and
Connectivity Modulate Pain Perception. J. Neurosci. 36, 5026–5033. doi:
10.1523/JNEUROSCI.3325-15.2016
Valentini, E., Torta, D. M., Mouraux, A., and Iannetti, G. D. (2011). Dishabituation
of laser-evoked EEG responses: dissecting the effect of certain and uncertain
changes in stimulus modality. J. Cogn. Neurosci. 23, 2822–2837. doi:
10.1162/jocn.2011.21609
Walton, K. D., Dubois, M., and Llinas, R. R. (2010). Abnormal thalamocortical
activity in patients with Complex Regional Pain Syndrome (CRPS) type I. Pain
150, 41–51. doi: 10.1016/j.pain.2010.02.023
Yeung, N., Botvinick, M. M., and Cohen, J. D. (2004). The neural basis of error
detection: conflict monitoring and the error-related negativity. Psychol. Rev.
111, 931. doi: 10.1037/0033-295x.111.4.931
Conflict of Interest Statement: The authors declare that the research was
conducted in the absence of any commercial or financial relationships that could
be construed as a potential conflict of interest.
Copyright © 2016 Spinelli and Nicolardi. This is an open-access article distributed
under the terms of the Creative Commons Attribution License (CC BY). The use,
distribution or reproduction in other forums is permitted, provided the original
author(s) or licensor are credited and that the original publication in this journal
is cited, in accordance with accepted academic practice. No use, distribution or
reproduction is permitted which does not comply with these terms.
Frontiers in Human Neuroscience | www.frontiersin.org 3 October 2016 | Volume 10 | Article 535


Crossref

Frontiers in Human Neuroscience

SPINELLI, GIUSEPPE

Archivio della ricerca- Università di Roma La Sapienza

GENERAL COMMENTARYpublished: 26 October 2016doi: 10.3389/fnhum.2016.00535Frontiers in Human Neuroscience | www.frontiersin.org 1 October 2016 | Volume 10 | Article 535Edited by:Vladimir Litvak,UCL Institute of Neurology, UKReviewed by:Michael X. Cohen,University of Amsterdam, Netherlands*Correspondence:Giuseppe Spinelligiuseppe.spinelli@uniroma1.itValentina Nicolardivalentina.nicolardi@uniroma1.it†These authors have contributedequally to this work.Received: 10 September 2016Accepted: 10 October 2016Published: 26 October 2016Citation:Spinelli G and Nicolardi V (2016)Commentary: Prestimulus ThetaOscillations and ConnectivityModulate Pain Perception.Front. Hum. Neurosci. 10:535.doi: 10.3389/fnhum.2016.00535Commentary: Prestimulus ThetaOscillations and ConnectivityModulate Pain PerceptionGiuseppe Spinelli 1, 2*† and Valentina Nicolardi 1, 2*†1Department of Psychology, Sapienza University of Rome, Rome, Italy, 2 IRCCS Santa Lucia Foundation, Rome, ItalyKeywords: feedback processing, gamma oscillations, pain perception, salience processing, theta oscillationsA commentary onPrestimulus Theta Oscillations and Connectivity Modulate Pain Perceptionby Taesler, P., and Rose, M., (2016). J. Neurosci. 36, 5026–5033. doi: 10.1523/JNEUROSCI.3325-15.2016Pain experience includes the fine-grain integration of both attentive and automatic (bottom-up;Legrain et al., 2012), as well as affective and intentional (top-down; Buschman and Miller, 2007)processes. While the neural underpinnings of post-stimulus pain processing have been deeplyexplored (Hauck et al., 2008), the oscillatory brain activity preceding pain processing is less farinvestigated.In a recent issue of Journal of Neuroscience, Taesler and Rose (2016) addresses this topic byrecording EEG from healthy participants who were forced to judge as “painful” or “non-painful”series of electrical stimulations delivered on their own left-hand. Painful stimulation was elegantlykept constant at the painful-threshold of each participant, and a subtractive approach (“painful”minus “non-painful” trials) was adopted to study the EEG signatures underlying pain processing.Results revealed enhanced pre-stimulus theta and gamma activity. Specifically, pre-stimulustheta power was both increased and decreased over fronto-temporal ipsilateral and contralateralelectrodes, respectively. Instead, pre-stimulus gamma power was enhanced over frontal andtemporal electrodes. Tellingly, while the ipsilateral reduction of theta-band power paralleled adecreased theta-band connectivity over frontal-lateral electrodes, the contralateral increase resultedin an enhanced connectivity of a bilateral fronto-temporal/centro-parietal network. Also, theconnectivity-pattern of the gamma increased between Fz and a parieto-temporal cluster around P6.Interestingly, source-analysis revealed likely generators in the bilateral insular cortex and posteriorcingulate cortex for the theta, and contralateral insular cortex for the gamma band.While this paper provides interesting and novel findings, we believe that these results deserveto be further discussed and interpreted in view of (i) the state-of-art literature of pain, and (ii)an integrated neurocognitive model of that takes into account both pain and negative-feedbackprocessing.First, the core of discussion of the authors aims at interpreting pre-stimulus theta oscillations asthe vehicle by which both contra- and ipsi-lateral insular cortices communicate to process painfulstimulation. This relevant result is compared to two previous studies (Sarnthein et al., 2006;Waltonet al., 2010) on chronic-pain patients, in which, however, only post-stimulus theta oscillations wererelated to pain processing. Thus, while Taesler and Rose provided relevant additions to the literatureon pain processing, a direct comparison with these latter studies is still difficult to be assessedgiven the different neurocognitive mechanisms underlying the processing of pain in individualswith chronic sensitization respect to healthies (Bushnell et al., 2013).Spinelli and Nicolardi Prestimulus Theta Modulate Pain PerceptionMoreover, the pre-stimulus theta-band power increase canbe viewed from a different perspective when considering thatthe paradigm of Taesler and Rose, by delivering in each triala constant painful stimulation after a fixation-cross, inducesa strong “stimulus–stimulus” association. This trial-by-trial“stimulus–stimulus” reinforcement, can induce an expectancy ofpain thatmight lead the neurocognitive system of pain processingto be active before the onset of the actual painful stimulation.Such an affective and anticipatory activation is in keeping withprevious evidences (Palermo et al., 2015; Sawamoto et al., 2000)showing that expectation of pain amplifies brain responses tothe somatosensory stimulation and activates mainly the anteriorcingulate cortex and insular cortices.Consequently, given that both insular cortices and variousregions of the middle-frontal cortex (Ridderinkhof et al.,2004), are linked to pre- and post-conflict monitoring (Yeunget al., 2004), feedback-monitoring and reinforcement-learning(Holroyd and Coles, 2002) via increasing theta band oscillations(Cohen, 2014), we argue that the pain processing system canshare the same temporal dynamics as the performance (andconflict) monitoring system (Shackman et al., 2011). In fact,it is worth noting how in Taesler and Rose the displacementof theta oscillations from pre- to post-stimulus, evolvesfrom insular cortices to fronto-central and dorso-lateralones. In this view, we suggest that the temporal dynamicsof processing painful stimulation can develop from an earlyaffective, orienting/salience response to unpleasant/unfavorableoutcomes—processed by right and left insular corticesprior to painful stimulation—to a late processing of theunfavorable/painful outcome itself—processed by frontalregions after painful stimulation. Accordingly, the theta-relatedconnectivity pattern showed by Taesler and Rose, seems toresemble the pattern of activation usually found when theso-called “saliency network”—mostly governed by the anteriorinsular cortex—attempt to elicit a (re)orienting responsebefore negative outcomes. In fact, it is arguably known howthe activation of the anterior insular activity, by signaling anincreased likelihood to receive unfavorable outcomes, aims atrapidly calling for additional cognitive control or behavioraladjustment (Klein et al., 2007). Thus, considering that in Taeslerand Rose, participants were always stimulated at their ownpainful threshold, the activity in the insular cortices couldhave governed, via theta increase, two different processes,namely: (i) the integration of personally/motivationallyinformation linked to painful stimulation and (ii) thepreparatory allocation of cognitive and physical resourcesof salience processing. While the latter is in keeping withprevious evidence (Sridharan et al., 2008), the former can beaddressed to the notion that pain-related cortical responsesreflect the processing of saliency of painful stimulations thatis related to a salience-specific multimodal neural activityrather than pain-specific unimodal neural response (Valentiniet al., 2011). However, studies investigating this latter issue inthe pre-stimulus interval are still missing, and further effortis needed to explore the link between these two cognitiveprocesses and the underlying electro-cortical signatures of painprocessing.Contrarily, the later stage of pain detection and the post-stimulus theta synchronization over middle-frontal and parieto-occipital brain regions, has been less discussed by the authors.It is worth mentioning that the pre-stimulus theta activationover the bi-lateral insular cortices shifts over fronto-centralscalp location during the post-stimulus processing. Interestingly,such an increase over mid-frontal electrodes might be linkedto the neurophysiological coding of: (i) individual psychologicaltraits during processing of painful stimuli (Schulz et al., 2012),and (ii) negative outcome monitoring related to a recruitmentof top-down cognitive processes to ultimately adapt futurebehavior. This latter hypothesis needs to be tested as itcould represent a valid integration of the saliency-processingtheory (Iannetti and Mouraux, 2010) and the performance-monitoring model. In this view, painful stimulation mightbe processed by the brain in the same way as negativefeedback/outcome (Shackman et al., 2011), and its detectionand encoding may be reflected in a coupling betweenpost-stimulus theta-gamma oscillations, where theta mightbe considered an high-level/ cognitive cortical marker ofmismatch detection, and the gamma a low-level/perceptualneural signature of the saliency and the intensity of painprocessing, respectively.Concluding, Taesler and Rose provided optimal evidences todeepen the functional significance of theta oscillations evokedbefore and after painful stimulation. Based on our argumentswe also believe that future investigations should focus on anintegrative neuro-cognitive model of pain perception that shouldtake into account also negative/unpleasant outcome monitoring,performance monitoring models, and their underlying electro-cortical signatures.AUTHOR CONTRIBUTIONSGS and VN equally contributed to read, comment, and write thecommentary.ACKNOWLEDGMENTSThe authors are grateful to Prof. Salvatore Maria Aglioti for hiscomments.REFERENCESBuschman, T. J., and Miller, E. K. (2007). Top-down versus bottom-up controlof attention in the prefrontal and posterior parietal cortices. Science 315,1860–1862. doi: 10.1126/science.1138071Bushnell, M. C., Ceko, M., and Low, L. A. (2013). Cognitive and emotional controlof pain and its disruption in chronic pain. Nat. Rev. Neurosci. 14, 502–511. doi:10.1038/nrn3516Cohen, M. X. (2014). A neural microcircuit for cognitive conflict detection andsignaling. Trends Neurosci. 37, 480–490. doi: 10.1016/j.tins.2014.06.004Frontiers in Human Neuroscience | www.frontiersin.org 2 October 2016 | Volume 10 | Article 535Spinelli and Nicolardi Prestimulus Theta Modulate Pain PerceptionHauck, M., Lorenz, J., and Engel, A. K. (2008). Role of synchronized oscillatorybrain activity for human pain perception. Rev. Neurosci. 19, 441–450. doi:10.1515/REVNEURO.2008.19.6.441Holroyd, C. B., and Coles, M. G. (2002). The neural basis of human errorprocessing: reinforcement learning, dopamine, and the error-related negativity.Psychol. Rev. 109, 679. doi: 10.1037/0033-295x.109.4.679Iannetti, G. D., and Mouraux, A. (2010). From the neuromatrix to the painmatrix (and back). Exp. Brain Res. 205, 1–12. doi: 10.1007/s00221-010-2340-1Klein, T. A., Endrass, T., Kathmann, N., Neumann, J., von Cramon, D. Y., andUllsperger, M. (2007). Neural correlates of error awareness. Neuroimage 34,1774–1781. doi: 10.1016/j.neuroimage.2006.11.014Legrain, V., Mancini, F., Sambo, C. F., Torta, D. M., Ronga, I., andValentini, E. (2012). Cognitive aspects of nociception and pain: bridgingneurophysiology with cognitive psychology. Neurophysiol. Clin. 42, 325–336.doi: 10.1016/j.neucli.2012.06.003Palermo, S., Benedetti, F., Costa, T., and Amanzio, M. (2015). Pain anticipation: anactivation likelihood estimation meta-analysis of brain imaging studies. Hum.Brain Mapp. 36, 1648–1661. doi: 10.1002/hbm.22727Ridderinkhof, K. R., Ullsperger, M., Crone, E. A., and Nieuwenhuis, S. (2004). Therole of the medial frontal cortex in cognitive control. Science 306, 443–447. doi:10.1126/science.1100301Sarnthein, J., Stern, J., Aufenberg, C., Rousson, V., and Jeanmonod, D.(2006). Increased EEG power and slowed dominant frequency inpatients with neurogenic pain. Brain 129, 55–64. doi: 10.1093/brain/awh631Sawamoto, N., Honda, M., Okada, T., Hanakawa, T., Kanda, M., Fukuyama,H., et al. (2000). Expectation of pain enhances responses to nonpainfulsomatosensory stimulation in the anterior cingulate cortex and parietaloperculum/posterior insula: an event-related functional magnetic resonanceimaging study. J. Neurosci. 20, 7438–7445. doi: 10.11501/3183115Shackman, A. J., Salomons, T. V., Slagter, H. A., Fox, A. S., Winter, J. J.,and Davidson, R. J. (2011). The integration of negative affect, pain andcognitive control in the cingulate cortex. Nat. Rev. Neurosci. 12, 154–167. doi:10.1038/nrn2994Sridharan, D., Levitin, D. J., and Menon, V. (2008). A critical role forthe right fronto-insular cortex in switching between central-executive anddefault-mode networks. Proc. Natl. Acad. Sci. U.S.A. 105, 12569–12574. doi:10.1073/pnas.0800005105Schulz, E., Tiemann, L., Witkovsky, V., Schmidt, P., and Ploner, M. (2012).γ Oscillations are involved in the sensorimotor transformation of pain. J.Neurophysiol. 108, 1025–1031. doi: 10.1152/jn.00186.2012Taesler, P., and Rose, M. (2016). Prestimulus Theta Oscillations andConnectivity Modulate Pain Perception. J. Neurosci. 36, 5026–5033. doi:10.1523/JNEUROSCI.3325-15.2016Valentini, E., Torta, D. M., Mouraux, A., and Iannetti, G. D. (2011). Dishabituationof laser-evoked EEG responses: dissecting the effect of certain and uncertainchanges in stimulus modality. J. Cogn. Neurosci. 23, 2822–2837. doi:10.1162/jocn.2011.21609Walton, K. D., Dubois, M., and Llinas, R. R. (2010). Abnormal thalamocorticalactivity in patients with Complex Regional Pain Syndrome (CRPS) type I. Pain150, 41–51. doi: 10.1016/j.pain.2010.02.023Yeung, N., Botvinick, M. M., and Cohen, J. D. (2004). The neural basis of errordetection: conflict monitoring and the error-related negativity. Psychol. Rev.111, 931. doi: 10.1037/0033-295x.111.4.931Conflict of Interest Statement: The authors declare that the research wasconducted in the absence of any commercial or financial relationships that couldbe construed as a potential conflict of interest.Copyright © 2016 Spinelli and Nicolardi. This is an open-access article distributedunder the terms of the Creative Commons Attribution License (CC BY). The use,distribution or reproduction in other forums is permitted, provided the originalauthor(s) or licensor are credited and that the original publication in this journalis cited, in accordance with accepted academic practice. No use, distribution orreproduction is permitted which does not comply with these terms.Frontiers in Human Neuroscience | www.frontiersin.org 3 October 2016 | Volume 10 | Article 535

Commentary: Prestimulus theta oscillations and connectivity modulate pain perception

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