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S50-5 Pain processing and cortical oscillations
29th International Congress of Clinical Neurophysiology S50-2 Motor cortex stimulation and pain perception Y. Tamura1 1 Department of Neurology, Sato Hospital, Utsunomiya, Japan A number of studies have been reported to show the neural substrates involved in the process of pain perception. For example, the primary and secondary somatosensory cortices, the anterior cingulate cortex, insular cortex, medial temporal cortices are known to play a pivotal role in pain perception. In addition to those cortices the primary motor cortex (M1) also plays a certain role in pain alleviation. Centrifugal gating with motor action toward noxious signals well demonstrates the role of M1. Besides epidural electrical stimulation of M1 was proven to have a beneficial effect on chronic intractable pain, and further, repetitive transcranial magnetic stimulation (rTMS) over M1 has also been attempted to alleviate pain. Several studies have been reported with some difference in stimulation parameters, and the results of its efficacy were inconsistent among those studies. Nevertheless, rTMS is still one therapeutic option for chronic pain, because it can be used noninvasively. Now this non-invasive technique has given us an opportunity to reconsider the role of M1 in the mechanisms of pain perception. Several imaging and physiological studies showed the relationship between M1 stimulation and functional changes in the anterior cingulate cortex. This connectivity may have a key role in the pain alleviation mechanisms. S50-3 Cortical mechanism of pain perception L. Garcia-Larrea1 1 Central Integration of Pain Unit France
U879 Inserm and University of Lyon,
Although neither electrophysiological nor imaging studies yield a complete account of the diversity of human pain, both techniques suggest a widely distributed “cortical pain matrix” (PM) with sequential vs simultaneous activities, and obligatory vs facultative components. The suprasylvian operculo-insular cortex is primary implicated in sensorial aspects of pain processing. Within this region, intracranial recordings suggest that the opercular region and the insula have different stimulusresponse curves, the operculum being more apt for encoding low levels of stimulus intensity, and the posterior insula better adapted to encode supra-threshold stimuli. These key-regions for sensory processing are also sensitive to cognitive load: thus, attention to pain significantly enhances opercular-insular responses, which are in turn reduced during distraction from pain. The activation of primary sensory, operculoinsular and mid-cingulate cortices is virtually simultaneous, although the functional contribution of each region to the pain experience is different. The cingulate contribution to phasic pain responses probably subserves orienting and withdrawal reactions, rather than emotional components. Experimental pain usually does not yield activation of emotion-related limbic/paralimbic regions, probably because over-protected contexts tend to minimise aversive components. The time-course of limbic activation is probably inappropriate for EPs or blood-flow based studies, but limbic activation can be obtained if emotional components (fear, anxiety) are specifically modulated. Activity of limbic regions is altered in patients with chronic pain, and can return to normal after analgesic interventions. The “basic pain matrix” is probably necessary for a somatic pain sensation to develop, but not sufficient to support the complete pain experience, which depends of memory processes that are contextdependent and can be modulated by emotions without changes in the PM. One example is the increased pain intensity felt when observing other people’s pain (“compassional hyperalgesia”). S50-4 Generators of laser evoked potentials M. Valeriani1,2 1 Division of Neurology, Ospedale Pediatrico Bambino Ges` u, Rome, Italy, 2 Faculties of Engineering, Science and Medicine, Aalborg University, Denmark Laser evoked potentials (LEPs) represent the most reliable technique for the functional assessment of the human nociceptive system. The main LEP component is represented by a biphasic negative-positive complex (N2/P2) having its largest amplitude on the Cz vertex. After hand stimulation, the N2 and P2 potentials show mean latencies of 200 ms and 350 ms, respectively. A middle-latency N1 potential is recorded with
S71 a mean latency of 150 ms on the temporal region contralateral to the stimulation. At the same latency, a positive P1 response is evoked on the frontal region. LEP generators have been studied by means of dipolar modeling of either the EEG or the MEG signal. Most studies agree in considering the bilateral opercular cortex and the anterior cingulate cortex (ACC) as the main generators of the scalp LEPs. In particular the N1 potential is thought to be generated by the second somatosensory (SII) area contralateral to the stimulation, while the ACC probably gives the most important contribution to the N2/P2 complex. This has been confirmed by studies of intracerebral LEP recording. Other cerebral areas, such as insular cortex, amygdala, posterior parietal region, frontal cortex, have been claimed to have a role in LEP building, but their involvement remains uncertain. A very interesting issue is represented by the possible contribution of the primary somatosensory (SI) area to LEPs. Although this represents a still unsolved problem, there are evidences suggesting that the area 3b (SI proper) is not activated by laser pulses. This does not exclude that other SI subareas, namely area 1 or area 2, may contribute to LEP generation. S50-5 Pain processing and cortical oscillations A. Schnitzler1 1 Institute of Clinical Neuroscience and Medical Psychology, and Department of Neurology, Heinrich-Heine-University Duesseldorf, Duesseldorf, Germany Oscillatory brain activity reflects an essential communication mechanism in the brain that is modulated during pain processing. In recent years pain-induced changes in oscillatory activity have been increasingly studied with MEG and EEG to investigate cortical processing of pain. This talk reviews human studies demonstrating the following findings: Focally applied selective painful stimulus suppress spontaneous oscillations in somatosensory, motor and visual areas probably reflecting the alerting function of pain. Gamma oscillations in primary somatosensory cortex are associated with subjective pain perception and increase with directed attention. Pain stimuli can elicit an involuntary shift of gamma oscillations from the visual system to somatosensory areas. These findings suggest that pain-induced gamma oscillations may be instrumental in amplifying pain-related signals and in enhancing their further processing in downstream cortical areas. 15 30 Hz oscillations were found in the posterior mid-cingulate and dorsal posterior cingulate cortex. These oscillations are not related to perceptual processing of noxious stimulus but may signify a transient cortical inhibition and aid in suppression of involuntary or voluntary motor programs primed by noxious stimulation. Taken together, analysis of pain-induced cortical oscillatory activity opens a new window towards the understanding of the neural substrates of pain and may be well suited to study pathological alterations of pain processing in chronic pain states. S50-6 Itch perception H. Mochizuki1,2 1 Department of Neurophysiology, CBTM, University of Heidelberg, Germany, 2 Department of Integrative Physiology, National Institute for Physiological Sciences, Japan Itch is unpleasant sensation with the desire to scratch. More than a decade ago, little was understood about brain mechanism of itch. Recently, functional neuroimaging studies using positron emission tomography (PET), functional magnetic resonance imaging (fMRI), electroencephalography (EEG) and magnetoencephalography (MEG) have investigated brain mechanism of itch. PET and fMRI studies identified brain regions activated by itch stimuli such as the prefrontal cortex, motor-related areas, somatosensory cortex, parietal cortex, cingulate cortex, insula, striatum, thalamus and cerebellum. It was reported that the posterior part of the cingulate cortex and insula were more selective for itch than pain whereas the thalamus, secondary somatosensory cortex (SII), amygdale and subgenual anterior cingulate cortex were more selective for pain than itch, speculating that such differences in selectivity may partly be associated with difference in perception between itch and pain. In addition, it was also reported that activation evoked by itch stimuli in the striatum associated with motor control and reward was significantly higher in atopic patients than normal controls. Based on the finding, it is speculated that uncontrollable scratching behavior known as itch-scratch-cycle in atopic patients may partly be
U879 Inserm and University of Lyon,
Although neither electrophysiological nor imaging studies yield a complete account of the diversity of human pain, both techniques suggest a widely distributed “cortical pain matrix” (PM) with sequential vs simultaneous activities, and obligatory vs facultative components. The suprasylvian operculo-insular cortex is primary implicated in sensorial aspects of pain processing. Within this region, intracranial recordings suggest that the opercular region and the insula have different stimulusresponse curves, the operculum being more apt for encoding low levels of stimulus intensity, and the posterior insula better adapted to encode supra-threshold stimuli. These key-regions for sensory processing are also sensitive to cognitive load: thus, attention to pain significantly enhances opercular-insular responses, which are in turn reduced during distraction from pain. The activation of primary sensory, operculoinsular and mid-cingulate cortices is virtually simultaneous, although the functional contribution of each region to the pain experience is different. The cingulate contribution to phasic pain responses probably subserves orienting and withdrawal reactions, rather than emotional components. Experimental pain usually does not yield activation of emotion-related limbic/paralimbic regions, probably because over-protected contexts tend to minimise aversive components. The time-course of limbic activation is probably inappropriate for EPs or blood-flow based studies, but limbic activation can be obtained if emotional components (fear, anxiety) are specifically modulated. Activity of limbic regions is altered in patients with chronic pain, and can return to normal after analgesic interventions. The “basic pain matrix” is probably necessary for a somatic pain sensation to develop, but not sufficient to support the complete pain experience, which depends of memory processes that are contextdependent and can be modulated by emotions without changes in the PM. One example is the increased pain intensity felt when observing other people’s pain (“compassional hyperalgesia”). S50-4 Generators of laser evoked potentials M. Valeriani1,2 1 Division of Neurology, Ospedale Pediatrico Bambino Ges` u, Rome, Italy, 2 Faculties of Engineering, Science and Medicine, Aalborg University, Denmark Laser evoked potentials (LEPs) represent the most reliable technique for the functional assessment of the human nociceptive system. The main LEP component is represented by a biphasic negative-positive complex (N2/P2) having its largest amplitude on the Cz vertex. After hand stimulation, the N2 and P2 potentials show mean latencies of 200 ms and 350 ms, respectively. A middle-latency N1 potential is recorded with
S71 a mean latency of 150 ms on the temporal region contralateral to the stimulation. At the same latency, a positive P1 response is evoked on the frontal region. LEP generators have been studied by means of dipolar modeling of either the EEG or the MEG signal. Most studies agree in considering the bilateral opercular cortex and the anterior cingulate cortex (ACC) as the main generators of the scalp LEPs. In particular the N1 potential is thought to be generated by the second somatosensory (SII) area contralateral to the stimulation, while the ACC probably gives the most important contribution to the N2/P2 complex. This has been confirmed by studies of intracerebral LEP recording. Other cerebral areas, such as insular cortex, amygdala, posterior parietal region, frontal cortex, have been claimed to have a role in LEP building, but their involvement remains uncertain. A very interesting issue is represented by the possible contribution of the primary somatosensory (SI) area to LEPs. Although this represents a still unsolved problem, there are evidences suggesting that the area 3b (SI proper) is not activated by laser pulses. This does not exclude that other SI subareas, namely area 1 or area 2, may contribute to LEP generation. S50-5 Pain processing and cortical oscillations A. Schnitzler1 1 Institute of Clinical Neuroscience and Medical Psychology, and Department of Neurology, Heinrich-Heine-University Duesseldorf, Duesseldorf, Germany Oscillatory brain activity reflects an essential communication mechanism in the brain that is modulated during pain processing. In recent years pain-induced changes in oscillatory activity have been increasingly studied with MEG and EEG to investigate cortical processing of pain. This talk reviews human studies demonstrating the following findings: Focally applied selective painful stimulus suppress spontaneous oscillations in somatosensory, motor and visual areas probably reflecting the alerting function of pain. Gamma oscillations in primary somatosensory cortex are associated with subjective pain perception and increase with directed attention. Pain stimuli can elicit an involuntary shift of gamma oscillations from the visual system to somatosensory areas. These findings suggest that pain-induced gamma oscillations may be instrumental in amplifying pain-related signals and in enhancing their further processing in downstream cortical areas. 15 30 Hz oscillations were found in the posterior mid-cingulate and dorsal posterior cingulate cortex. These oscillations are not related to perceptual processing of noxious stimulus but may signify a transient cortical inhibition and aid in suppression of involuntary or voluntary motor programs primed by noxious stimulation. Taken together, analysis of pain-induced cortical oscillatory activity opens a new window towards the understanding of the neural substrates of pain and may be well suited to study pathological alterations of pain processing in chronic pain states. S50-6 Itch perception H. Mochizuki1,2 1 Department of Neurophysiology, CBTM, University of Heidelberg, Germany, 2 Department of Integrative Physiology, National Institute for Physiological Sciences, Japan Itch is unpleasant sensation with the desire to scratch. More than a decade ago, little was understood about brain mechanism of itch. Recently, functional neuroimaging studies using positron emission tomography (PET), functional magnetic resonance imaging (fMRI), electroencephalography (EEG) and magnetoencephalography (MEG) have investigated brain mechanism of itch. PET and fMRI studies identified brain regions activated by itch stimuli such as the prefrontal cortex, motor-related areas, somatosensory cortex, parietal cortex, cingulate cortex, insula, striatum, thalamus and cerebellum. It was reported that the posterior part of the cingulate cortex and insula were more selective for itch than pain whereas the thalamus, secondary somatosensory cortex (SII), amygdale and subgenual anterior cingulate cortex were more selective for pain than itch, speculating that such differences in selectivity may partly be associated with difference in perception between itch and pain. In addition, it was also reported that activation evoked by itch stimuli in the striatum associated with motor control and reward was significantly higher in atopic patients than normal controls. Based on the finding, it is speculated that uncontrollable scratching behavior known as itch-scratch-cycle in atopic patients may partly be