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

Mechanisms of human nociception can be studied by the use of CO2 laser stimulation, which selectively activates nociceptive receptors, and by the use of various noninvasive techniques. In addition to the contralateral thalamus, at least several cortical areas including the contralateral SI, bilateral SII, anterior cingulated cortex, and insular cortices are involved in the pain sensation/perception. Pain perception (Fig. 8) is unique because these cortical structures seem to be activated in parallel at nearly the same latency after the stimulus presentation. SI seems to play a role in basic pain processing while SII and insula are involved in higher functions of pain perception. Emotional aspects of pain perception are mediated by anterior cingulate cortex and posterior insula/parietal operculum.
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PMID:Central mechanisms of pain perception. 1610 4

We recorded magnetoencephalography (MEG) and functional magnetic resonance imaging (fMRI) following noxious laser stimulation in a Yoga Master who claims not to feel pain when meditating. As for background MEG activity, the power of alpha frequency bands peaking at around 10 Hz was much increased during meditation over occipital, parietal and temporal regions, when compared with the non-meditative state, which might mean the subject was very relaxed, though he did not fall asleep, during meditation. Primary pain-related cortical activities recorded from primary (SI) and secondary somatosensory cortices (SII) by MEG were very weak or absent during meditation. As for fMRI recording, there were remarkable changes in levels of activity in the thalamus, SII-insula (mainly the insula) and cingulate cortex between meditation and non-meditation. Activities in all three regions were increased during non-meditation, similar to results in normal subjects. In contrast, activities in all three regions were weaker during meditation, and the level was lower than the baseline in the thalamus. Recent neuroimaging and electrophysiological studies have clarified that the emotional aspect of pain perception mainly involves the insula and cingulate cortex. Though we cannot clearly explain this unusual condition in the Yoga Master, a change of multiple regions relating to pain perception could be responsible, since pain is a complex sensory and emotional experience.
Eur J Pain 2005 Oct
PMID:Intracerebral pain processing in a Yoga Master who claims not to feel pain during meditation. 1613 87

Somatosensory and pain responses to direct intracerebral stimulations of the SII area were obtained in 14 patients referred for epilepsy surgery. Stimulations were delivered using transopercular electrodes exploring the parietal opercular cortex (SII area), the suprasylvian parietal cortex (SI area) and the insular cortex. SII responses were compared to those from adjacent SI and insular cortex. In the three areas we elicited mostly somatosensory responses, including paresthesiae, temperature and pain sensations. The rate of painful sensations (10%) was similar in SII and in the insula, while no painful sensation was evoked in SI. A few non-somatosensory responses were evoked by SII stimulation. Conversely various types of non-somatosensory responses (auditory, vegetative, vestibular, olfacto-gustatory, etc.) were evoked only by insular stimulation, confirming that SII, like SI, are mostly devoted to the processing of somatosensory inputs whereas the insular cortex is a polymodal area. We also found differences in size and lateralization of skin projection fields of evoked sensations between the three studied areas, showing a spatial resolution of the somatotopic map in SII intermediate between those found in SI and insula. This study shows the existence of three distinct somatosensory maps in the suprasylvian, opercular and insular regions, and separate pain representations in SII and insular cortex.
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PMID:Somatosensory and pain responses to stimulation of the second somatosensory area (SII) in humans. A comparison with SI and insular responses. 1617 70

Forebrain activation patterns in normal and spinal-injured Sprague-Dawley (SD) rats were determined by measuring regional cerebral blood flow as an indicator of neuronal activity. Data are compared to our previously published findings from normal and spinal-injured Long-Evans (LE) rats and reveal a striking degree of overlap, as well as differences, between strains in the basal (unstimulated) forebrain activation in normal animals. Specifically, 81% of the structures sampled showed similar activation in both strains, suggesting a consistent and identifiable pattern of basal cerebral activation in the rat. LE controls showed significantly greater basal activation in the remaining structures compared to SD control group, including the anterior dorsal thalamus, basolateral amygdala, SII cortex, and the hypothalamic paraventricular nucleus. In contrast, spinal cord injury (SCI) resulted in strain-specific changes in forebrain activation categorized by structures that showed significant increases in: (1) only LE SCI rats (posterior, ventrolateral, and ventroposterolateral thalamic nuclei); (2) only SD SCI rats (anterior-dorsal and medial thalamus, basolateral amygdala, cingulate and retrosplenial cortex, habenula, interpeduncular nucleus, hypothalamic paraventricular nucleus, periaqueductal gray); or (3) both strains (arcuate nucleus, ventroposteromedial thalamus, SI and SII somatosensory cortex). These results provide information related to the remote, i.e. supraspinal, effects of spinal cord injury and suggest that genetic differences play an important part in the forebrain response to such injury. Brain activation studies therefore provide a useful tool in understanding the full extent of secondary consequences following spinal injury and for identifying potential central mechanism responsible for the development of pain.
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PMID:Differences in forebrain activation in two strains of rat at rest and after spinal cord injury. 1618 86

We use fMRI to examine brain activity for pain elicited by palpating joints in a single patient suffering from psoriatic arthritis. Changes in these responses are documented when the patient ingested a single dose of a selective cyclooxygenase-2 inhibitor (COX-2i). We show that mechanical stimulation of the painful joints exhibited a cortical activity pattern similar to that reported for acute pain, with activity primarily localized to the thalamus, insular, primary and secondary somatosensory cortices and the mid anterior cingulum. COX-2i resulted in significant decreased in reported pain intensity and in brain activity after 1 hour of administration. The anterior insula and SII correlated with pain intensity, however no central activation site for the drug was detected. We demonstrate the similarity of the activation pattern for palpating painful joints to brain activity in normal subjects in response to thermal painful stimuli, by performing a spatial conjunction analysis between these maps, where overlap is observed in the insula, thalamus, secondary somatosensory cortex, and anterior cingulate. The results demonstrate that one can study effects of pharmacological manipulations in a single subject where the brain activity for a clinical condition is delineated and its modulation by COX-2i demonstrated. This approach may have diagnostic and prognostic utility.
Mol Pain 2005 Nov 02
PMID:Single subject pharmacological-MRI (phMRI) study: modulation of brain activity of psoriatic arthritis pain by cyclooxygenase-2 inhibitor. 1626 29

We investigated pain evoked activity in the human secondary sensory cortex (SII) following clonidine administration in six healthy volunteers using multi-channel magnetoencephalography (MEG). Pain was elicited by electrical shocks applied intracutaneously to the fingertip. Subjects rated pain intensity and perceptions of tiredness and passiveness by numerical ranking scales. Each subject underwent two investigations, one week apart from each other, with clonidine doses of 1.5 or 3.0microg/kg, administered intravenously in a random order and double-blinded. We applied a total number of seven blocks, each consisting of 60 painful stimuli, with one adaptation block, one pre-medication block, four post-medication blocks and one recovery block at the end of the session. MEG data were analysed by dipole reconstruction using CURRY(R) (Neuroscan, Hamburg) software package. Cortical activity in the contralateral SII cortex appeared with peak latencies of 118.5+/-10ms. This activity was significantly reduced by clonidine, in parallel with a reduction of pain intensity and enhancement of subjective tiredness and passiveness. There was, however, no significant correlation between MEG and subjective effects. Although both clonidine doses had similar effects, the higher dose induced longer changes. Results indicate that intravenous clonidine is able to relieve pain, but the exact mechanism of clonidine at the level of the SII cortex remains unclear. It is possible that clonidine interacts with the brainstem ascending system regulating vigilance and arousal which would explain the observed decrement of pain induced activity in SII. An additional more specific analgesic action at spinal level cannot be excluded.
Eur J Pain 2006 Nov
PMID:Clonidine effects on pain evoked SII activity in humans. 1643 73

Self-generated sensory stimulation can be distinguished from externally generated stimulation that is otherwise identical. To determine how the brain differentiates external from self-generated noxious stimulation and which structures of the lateral pain system use neural signals to predict the sensory consequences of self-generated painful stimulation, we used functional magnetic resonance imaging to examine healthy human subjects who received thermal-contact stimuli with noxious and non-noxious temperatures on the resting right hand in random order. These stimuli were internally (self-generated) or externally generated. Two additional conditions served as control conditions: to account for stimulus onset uncertainty, acoustic stimuli preceding the same thermal stimuli were used with variable or fixed delays but without any stimulus-eliciting movements. Whereas graded pain-related activity in the insula and secondary somatosensory cortex (SII) was independent of how the stimulus was generated, it was attenuated in the primary somatosensory cortex (SI) during self-generated stimulation. These data agree with recent concepts of the parallel processing of nociceptive signals to the primary and secondary somatosensory cortices. They also suggest that brain areas that encode pain intensity do not distinguish between internally or externally applied noxious stimuli, i.e., this adaptive biological mechanism prevents harm to the individual. The attenuated activation of SI during self-generated painful stimulation might be a result of the predictability of the sensory consequences of the pain-related action.
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PMID:Neural activity related to self- versus externally generated painful stimuli reveals distinct differences in the lateral pain system in a parametric fMRI study. 1645 10

To elucidate the role of somatosensory cortices in coding pain magnitude, we recorded the neuromagnetic responses of ten subjects to mild, moderate, and severe pain stimulation by delivering thulium-laser pulses on the dorsum of the left hand. The stimulus intensities for producing different pain levels were determined individually, and the mean values across subjects were 255, 365, and 490 mJ for mild, moderate, and severe pain, respectively. We obtained 40 responses for each intensity condition, and analyzed the averaged cortical signals by multi-dipole modeling. All subjects showed consistent activation over the bilateral secondary somatosensory (SII) cortices for each intensity level, peaking around 150-230 ms, with 15-ms earlier on the contralateral hemisphere. The SII dipole strength was significantly larger for the moderate than for the mild pain stimulation, but lacked further increase as the pain magnitude elevated to the severe level. In contrast, the primary somatosensory cortical response was detected in only half of our subjects, and thus it seemed difficult to evaluate its role in pain intensity coding. Our results suggest that activation strength in human SII cortices reflects the magnitude of peripheral noxious inputs only up to the moderate level, and some other cerebral correlates may get involved in sensing a further increment of pain magnitude.
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PMID:Neuromagnetic SII responses do not fully reflect pain scale. 1645 8

Main elements concerning the physiology of pain are described, as well as the structures of the nervous system at the origin of the central control of pain: peripheral fibres (small diameter myelinated A delta and unmyelinated C fibres); spinal ascending pathways; cerebral structures relaying nociceptive information (medial and ventro-postero-lateral thalamic relays); SI and SII cortical areas; spinal segmentary and supraspinal excitatory and inhibitory controls; diffuse noxious inhibitory controls (DNIC). Chronic pain is a result of two processes: peripheral and central sensitization, in relation with inflammation and nerve injury at peripheral level and with neuroplasticity at central level. Neurotrophins, mainly NGF and BDNF and their receptors (LNTR, TrkA and TrkB) are involved in these processes. Pain is a result of an unpleasant emotional experience: its various components, mainly the emotional one, may be increased or decreased considering the different characteristics of the stimulus and of the affective state of the patient, as well as the context in which this stimulus is applied. The role of physiological systems, unconnected with those classically involved in the physiology of nociception and pain, such as the motor cortex in phantom limb pain, are described in conclusion, to focus on the extreme complexity of the control systems of pain in humans.
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PMID:[Neural basis of pain]. 1655 14

The SII area and the posterior insular region are both activated by thermal stimuli in functional imaging studies. However, controversy remains as to a possible differential encoding of thermal intensity by each of these 2 contiguous areas. Using CO(2) laser stimulations, we analyzed the modifications induced by increasing thermal energy on evoked potentials recorded with electrodes implanted within SII and posterior insula in patients referred for presurgical evaluation of epilepsy. Although increasing stimulus intensities enhanced both SII and insular responses, the "dynamics" of their respective amplitude changes were different. SII responses were able to encode gradually the intensity of stimuli from sensory threshold up to a level next to pain threshold but tended to show a ceiling effect for higher painful intensities. In contrast, the posterior insular cortex failed to detect nonnoxious laser pulses but reliably encoded stimulus intensity variations at painful levels, without showing saturation effects for intensities above pain threshold. According to these results, one can assume that insular cortex could be more involved in the triggering of affective recognition of, and motor reaction to, noxious stimuli, whereas SII would be more dedicated to finer-grain discrimination of stimulus intensity, from nonpainful to painful levels.
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PMID:Human SII and posterior insula differently encode thermal laser stimuli. 1661 65


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