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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pain is processed in multiple brain areas, indicating the complexity of pain perception. The ability to locate pain plays a pivotal role in immediate defense and withdrawal behavior. However, how the brain localizes nociceptive information without additional information from somatotopically organized mechano-receptive pathways is not well understood. We used single-trial functional magnetic resonance imaging (fMRI) to assess hemodynamic responses to right and left painful stimulation. Thulium-YAG-(yttrium-aluminium-granate)-laser-evoked pain stimuli, without concomitant tactile component, were applied to either hand in a randomized order. A contralateral bias of the BOLD response was investigated to determine areas involved in the coding of the side of stimulation, which we observed in primary (SI) and secondary (SII) somatosensory cortex, insula, and the thalamus. This suggests that these structures provide spatial information of selective nociceptive stimuli. More importantly, this contralateral bias of activation allowed functionally segregated activations within the SII complex, the insula, and the thalamus. Only distinct subregions of the SII complex, the posterior insula and the lateral thalamus, but not the remaining SII complex, the anterior insula and the medial thalamus, showed a contralaterally biased representation of painful stimuli. This result supports the hypothesis that sensory-discriminative attributes of painful stimuli, such as those related to body side, are topospecifically represented within the forebrain projections of the nociceptive system and highlights the concept of functional segregation and specialization within these structures.
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PMID:Single trial fMRI reveals significant contralateral bias in responses to laser pain within thalamus and somatosensory cortices. 1266 51

Survivors of prolonged cerebral anoxia often remain in the persistent vegetative state (PVS). In this study, long-term PVS patients were investigated by 15O-H(2)O PET to analyze their central processing of pain. The study was approved by the local Ethics Committee, the experiments were performed in accordance with the Helsinki Declaration of 2000. Seven patients remaining in PVS of anoxic origin for a mean of 1.6 years (range 0.25-4 years) were investigated. We performed functional PET of the brain using 15O-labelled water during electrical nociceptive stimulation. Additionally, a brain metabolism study using 18F-fluorodeoxyglucose (FDG) PET and multi-sequence MRI (including a 3-D data set) were acquired in all patients. PET data were analyzed by means of Statistical Parametric Mapping (SPM99) and coregistered to a study-specific brain template. MRI and FDG PET showed severe cortical impairment at the structural and the functional level, that is, general atrophy of various degrees and a widespread significant hypometabolism, respectively. Pain-induced activation (hyperperfusion) was found in the posterior insula/secondary somatosensory cortex (SII), postcentral gyrus/primary somatosensory cortex (SI), and the cingulate cortex contralateral to the stimulus and in the posterior insula ipsilateral to the stimulus (P<0.05, small-volume-corrected). No additional areas of the complex pain-processing matrix were significantly activated. In conclusion, the regional activity found at the cortical level indicates that a residual pain-related cerebral network remains active in long-term PVS patients.
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PMID:Activation of a residual cortical network during painful stimulation in long-term postanoxic vegetative state: a 15O-H2O PET study. 1281 4

To better understand the antinociceptive effect of fluvoxamine, we measured regional cerebral blood flow during laser-evoked pain and hot sensations using H(2)15O positron emission tomography and also subjective pain and hot sensations before and after fluvoxamine or placebo administration for 7 days to 12 healthy volunteers. The subjectively rated pain score was significantly reduced by fluvoxamine administration. Painful stimuli activated multiple brain regions. After fluvoxamine administration the ipsilateral anterior cingulate cortex (ACC), contralateral insular cortex (IC), and contralateral secondary somatosensory cortex (SII) activations were reduced. The bilateral IC activation was also reduced in the placebo group. These results suggest that fluvoxamine specifically reduced activation of the ACC and SII, which are areas concerned with the affective and integrative components of pain.
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PMID:Fluvoxamine modulates pain sensation and affective processing of pain in human brain. 1285 34

A recent PET study revealed that the first and second somatosensory cortices (SI, SII), and the anterior cingulate cortex are activated by painful peripheral stimulation in humans. It has become clear that painful signals (nociceptive information) evoked at the periphery are transmitted via various circuits to the multiple cerebral cortices where pain signals are processed and perceived. Human or clinical pain is not merely a modality of somatic sensation, but associated with the affect that accompanies sensation. Consequently, pain has a somatosensory-discriminative aspect and an affective-cognitive aspect that are processed in different but correlated brain structures in the ascending circuits. Considering the physiologic characteristics and fiber connections, the SI and SII cortices appear to be involved in somatosensory-discriminative pain, and the anterior cingulate cortex (area 24) in the affective-cognitive aspect of pain. This paper deals with the ascending pain pathways from the periphery to these cortices and their interconnections. Our recent findings on the protease-activated receptors 1 and 2 (PAR-1, and -2), which are confirmed to exist in the dorsal root ganglion cells, are also described. Activation of PAR-2 during inflammation or tissue injury at the periphery is pronociceptive, while PAR-1 appears to be antinociceptive. Based on the these findings, PAR-1 and PAR-2 are attracting interest as target molecules for new drug development.
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PMID:[Pain information pathways from the periphery to the cerebral cortex]. 1287 36

We investigated the effects of sleep on pain-related somatosensory evoked magnetic fields (SEFs) following painful electrical stimulation to identify the mechanisms generating them in both fast A-beta fibers relating to touch and slow A-delta fibers relating to pain. While the subjects were awake, non-painful and painful electrical stimulations were applied, and while asleep, painful stimulation was applied to the left index finger. During awake, five components (1M-5M) were identified following both non-painful and painful stimulation, but the 4M and 5M at around 70-100 ms and 140-180 ms, respectively, were significantly enhanced following painful stimulation. During sleep, 1M and 2M generated in the primary somatosensory cortex (SI) did not show a significant change, 3M in SI showed a slight but significant amplitude reduction, and 4M and 5M generated in both SI and the secondary somatosensory cortex (SII) were significantly decreased in amplitude or disappeared. The 4M and 5M are complicated components generated in SI and SII ascending through both A-beta fibers and A-delta fibers. They are specifically enhanced by painful stimulation due to an increase of signals ascending through A-delta fibers, and are markedly decreased during sleep, because they much involve cognitive function.
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PMID:Effects of sleep on pain-related somatosensory evoked magnetic fields in humans. 1288 Sep 9

Converging lines of evidence confirm a role for the anterior parietal cortex in pain processing and extend the traditional view of SI to include discriminative aspects of somatic stimulation that is potentially tissue-damaging (e.g., painful). Recent studies more specifically implicate SI in the sensory aspect of pain perception by demonstrating that SI activation is modulated by cognitive manipulations that alter perceived pain intensity, but not by manipulations that alter unpleasantness, independent of pain intensity. Nevertheless, despite the probable role of SI in the encoding of the various sensory features of pain, considerable evidence suggests that nociceptive input to SI may also serve to modulate tactile perception. Thus, SI cortex may be involved in both the perception and modulation of both painful and nonpainful somatosensory sensations. Defining a role in pain processing for the parietal operculum is somewhat more problematic. The absence of a fine somatotopic organization of cutaneous (or visceral) receptors virtually eliminates a substantial role for this region in localizing noxious stimuli. Several studies suggest separate representations for pain and touch within the posterior parietal cortex and SII, respectively; however, inter-species differences in cortical anatomy and inconsistencies in the designation of SII proper preclude a clear reconciliation of the data. Likewise, suggestions that SII activation is predominantly related to processing the nociceptive quality of the stimulus (60,61) are inconsistent with many studies in both human and nonhuman subjects, which show a strong functional relationship between SII activity and innocuous (especially, vibrotactile) stimulation. Nevertheless, the numerous studies indicating pain-related activation within the parietal operculum (and/or SII) underscore the potential importance of this region in the perception of pain and the need for continued research. Finally, a possible role of posterior parietal cortex (BA 5/7, 39/40) in orientation and attention toward painful sensory stimuli is consistent with existing literature describing this region as a poly modal association area concerned with intrapersonal and extrapersonal space; however, results from studies that actually manipulate the subjects' level of attention relative to painful stimuli have not uniformly supported this hypothesis (75). Future studies assessing both attentional demand and direct manipulation or motor interactions involving noxious stimuli may help to resolve this issue. In spite of some discrepant results concerning specific details of the nociceptive process, the weight of human pain research now firmly establishes a role for the parietal lobes in the conscious appreciation of the sensation of pain.
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PMID:Is there a role for the parietal lobes in the perception of pain? 1289 2

The evidence presented by Craig and his colleagues for an important projection from lamina I spinothalamic tract neurons to a renamed thalamic nucleus (the posterior part of the ventral medial nucleus or VMpo), as well as to the ventrocaudal medial dorsal and the ventral posterior inferior thalamic nuclei, is critically reviewed. Of particular concern is the denial of an important nociceptive lamina I projection to the ventrobasal complex. Contrary evidence is reviewed that strongly favors a role of spinothalamic projections from both lamina I and deep layers of the dorsal horn to the ventrobasal complex and other thalamic nuclei and from there to the SI and SII somatosensory cortices in the sensory-discriminative processing of pain and temperature information.
J Pain 2002 Apr
PMID:A critical review of the role of the proposed VMpo nucleus in pain. 1462 96

The regional activity of the contralateral primary (SI) and the bilateral secondary (SII) somatosensory areas during median nerve stimulations at five intensity levels (ranging from nonpainful motor threshold to moderate pain) was studied by means of functional magnetic resonance imaging (fMRI). The aim was to characterize the functional topography of SII compared to SI as a function of the stimulus intensity. Results showed that the galvanic stimulation of the median nerve activated the contralateral SI at all stimulus intensities. When considered as a single region, SII was more strongly activated in the contralateral than in the ipsilateral hemisphere. When a finer spatial analysis of the SII responses was performed, the activity for the painful stimulation was localized more posteriorly compared to that for the nonpainful stimulation. This is the first report on such a SII segregation for transient galvanic stimulations. The activity (relative signal intensity) of this posterior area increased with the increase of the stimulus intensity. These results suggest a spatial segregation of the neural populations that process signals conveyed by dorsal column-medial lemniscus (nonpainful signals) and neospinothalamic (painful signals) pathways. Further fMRI experiments should evaluate the functional properties of these two SII subregions during tasks involving sensorimotor integration, learning, and memory demands.
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PMID:Functional topography of the secondary somatosensory cortex for nonpainful and painful stimuli: an fMRI study. 1464 73

The secondary somatosensory cortex (SII) is strongly involved in the processing of somatosensory tactile and nociceptive sensations. We investigated the effect on SII responses of simultaneous painful and nonpainful electrical stimulations delivered to the thumb and little finger. According to the "bimodal" (i.e., nociceptive, tactile) organization of SII, it was expected that simultaneous painful and nonpainful stimulations would lead to modality interference with a marked reduction ("gating") of somatosensory evoked fields (SEFs) generated in SII. Eight different stimulus conditions were studied. Two conditions were simultaneous "unimodal" (thumb and little finger nonpainful; thumb and little finger painful) and two conditions were simultaneous "bimodal" (thumb nonpainful and little finger painful; thumb painful and little finger nonpainful). As a reference, four conditions included stimulations at single sites (thumb nonpainful, little finger nonpainful, thumb painful, little finger painful). The gating phenomenon was defined as the percentage of difference between the intensities of SII activation after simultaneous compared to the sum of the separate stimulations. Results showed that simultaneous stimulations induced gating effects on SEFs generated by SII. No significant gating differences were observed after the two unimodal stimulations, suggesting a negligible effect of global energy on gating. Instead, the gating effects on bilateral SII activity were stronger after simultaneous bimodal when compared to unimodal stimulations. Our findings hint that there could be a greater level of integration/convergence of painful and nonpainful stimuli in SII with respect to SI. Future studies should explore if it could have an important role in exploring pain relief.
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PMID:"Gating" effects of simultaneous peripheral electrical stimulations on human secondary somatosensory cortex: a whole-head MEG study. 1464 80

In this work we review data on cortical generators of laser-evoked potentials (LEPs) in humans, as inferred from dipolar modelling of scalp EEG/MEG results, as well as from intracranial data recorded with subdural grids or intracortical electrodes. The cortical regions most consistently tagged as sources of scalp LERs are the suprasylvian region (parietal operculum, SII) and the anterior cingulate cortex (ACC). Variability in opercular sources across studies appear mainly in the anterior-posterior direction, where sources tend to follow the axis of the Sylvian fissure. As compared with parasylvian activation described in functional pain imaging studies, LEP opercular sources tended to cluster at more superior sites and not to involve the insula. The existence of suprasylvian opercular LEPs has been confirmed by both epicortical (subdural) and intracortical recordings. In dipole-modelling studies, these sources appear to become active less than 150 ms post-stimulus, and remain in action for longer than opercular responses recorded intracortically, thus suggesting that modelled opercular dipoles reflect a "lumped" activation of several sources in the suprasylvian region, including both the operculum and the insula. Participation of SI sources to explain LEP scalp distribution remains controversial, but evidence is emerging that both SI and opercular sources may be concomitantly activated by laser pulses, with very similar time courses. Should these data be confirmed, it would suggest that a parallel processing in SI and SII has remained functional in humans for noxious inputs, whereas hierarchical processing from SI toward SII has emerged for other somatosensory sub-modalities. The ACC has been described as a source of LEPs by virtually all EEG studies so far, with activation times roughly corresponding to scalp P2. Activation is generally confined to area 24 in the caudal ACC, and has been confirmed by subdural and intracortical recordings. The inability of most MEG studies to disclose such ACC activity may be due to the radial orientation of ACC currents relative to scalp. ACC dipole sources have been consistently located between the VAC and VPC lines of Talairach's space, near to the cingulate subsections activated by motor tasks involving control of the hand. Together with the fact that scalp activities at this latency are very sensitive to arousal and attention, this supports the hypothesis that laser-evoked ACC activity may underlie orienting reactions tightly coupled with limb withdrawal (or control of withdrawal). With much less consistency than the above-mentioned areas, posterior parietal, medial temporal and anterior insular regions have been occasionally tagged as possible contributors to LEPs. Dipoles ascribed to medial temporal lobe may be in some cases re-interpreted as being located at or near the insular cortex. This would make sense as the insular region has been shown to respond to thermal pain stimuli in both functional imaging and intracranial EEG studies.
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PMID:Brain generators of laser-evoked potentials: from dipoles to functional significance. 1467 42


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