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

An improved method is described for the quantitation of lidocaine and its dominant metabolites in rat plasma, 3-hydroxy-lidocaine glucuronide and 3-hydroxy-MEG-X glucuronide. Frozen plasma samples (100-200 microliters) were thawed and deproteinated by precipitation with acetonitrile, before the conversion of glucuronidates into their respective hydroxylated forms by acid hydrolysis. After extraction with solid-phase C18 cartridge chromatography, the metabolites and parent drug were analyzed by capillary gas chromatography-nitrogen phosphorus detection, without derivativization. A detection limit of 0.005 microgram/ml for lidocaine and nonglucuronidated metabolites and 0.01 microgram/ml for glucuronidated metabolites was achieved. The method offers significant improvements in sensitivity relative to existing techniques, which should be of specific benefit to studies in which sample volume is limited, such as those concerned with the pharmacokinetics of lidocaine metabolism in small-animal pain state models.
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PMID:An improved method for the measurement of lidocaine and its metabolites in rat plasma. 910 47

Pain perception in the brain can be analyzed by neuroimaging (PET, fMRI) and electrophysiological parameter mapping (EEG, ERP/MEG, MEF). These studies have generally been focused on the localization of cerebral activation. Whether pain can be conceptualized as localized function or best be understood by distributed function is important to the theory of human pain processing in the brain. Here, we report that cold and pain perception in the brain is characterized by webs of EEG coherence changes which may reflect coupling or de-coupling of different cortical areas during cold and pain processing. EEG was recorded during cold and pain perception (right hand immersion in 15 degrees C cool-water vs. 0.3 degrees C ice-water for 3 min.) with eyes opened. Subjects rated the cold perception at 2.3 (cool to cold, but no pain) and the pain perception at 6.7 (moderate-strong pain) in a 1-10 scale. The obtained EEG spectral parameters were compared with the corresponding parameters of the resting baseline using paired Wilcoxon tests in the sense of statistical filters to depict those differences which differ clearly from changes by chance. The results were presented in probability maps. The EEG results indicated highly differential coherence networks between cold and pain perception. The cold perception was characterized as decreased coherence in the theta band mainly between frontal electrodes and increased interhemispheric coherence in the alpha range mainly between central and frontal positions. During pain perception almost no coherence changes in the theta band were observed, but great coherence increase in the delta band between central, parietal and frontal electrodes. The network of coherence changes in the alpha band showed strong involvement of electrode C3 concerning coherence increases with frontal positions. In the beta-1 band coherence increase within the left hemisphere was much more pronounced during pain than during cold. The differential characteristics of EEG coherence changes based on neural networks and their spatial organization in the neocortex indicate the distributed brain processing between cold and pain perception in man. This study may contribute to our understanding of the large scale neural networks in cognition based on neurophysiological binding hypothesis and network connections of neural ensembles.
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PMID:Topology of EEG coherence changes may reflect differential neural network activation in cold and pain perception. 988 Jan 70

New developments in brain imaging lead to a better understanding of cortical and subcortical processes involved in pain perception and the establishment of chronic pain. For different forms of chronic pain long-term changes in cortical structures have been described. In patients with phantom limb pain and back pain alterations in the somatotopic organization of the primary somatosensory (SI) could be observed. The amount of this reorganization is correlated with the subjective pain rating. These changes, which are based on processes of neuronal plasticity, can partially be reversed by analgesic interventions. For the investigation of cortical processes concerning reorganization, EEG and MEG methods are most suitable because of their high temporal and spatial resolution. In conclusion, these findings open a new way for therapeutic interventions to prevent the development of chronic pain.
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PMID:Neuroimaging of chronic pain: phantom limb and musculoskeletal pain. 1102 25

Imaging techniques with high spatial and temporal resolution (PET,fMRI, MEG) provide detailed information about the brains' processing of pain. Structures detected by these techniques are not understood as pain centers but as nodal points of a dynamic network which is influenced by physiological and psychological input. Imaging techniques can be used for the investigation of different pain components. The neuronal network that encodes sensory-discriminative information consists of the primary and secondary somatosensory cortex which receive input from lateral thalamic nuclei. Information for the affective pain component reach the anterior cingulate cortex, insula and prefrontal cortex via medial thalamic nuclei. Until now only little is known about cortical structures mediating the cognitive pain component. In chronic pain the cortical and subcortical processing of nociceptive input is presumably modified. Reorganization in the primary somatosensory cortex is presented as an example of neuronal plasticity induced by chronic pain.
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PMID:[Neural networks and pain processing. New insights from imaging techniques]. 1122 Feb 53

With the maturation of EEG/MEG brain mapping and PET/fMRI neuroimaging in the 1990s, greater understanding of pain processing in the brain now elucidates and may even challenge the classical theory of pain mechanisms. This review scans across the cultural diversity of pain expression and modulation in man. It outlines the difficulties in defining and studying human pain. It then focuses on methods of studying the brain in experimental and clinical pain, the cohesive results of brain mapping and neuroimaging of noxious perception, the implication of pain research in understanding human consciousness and the relevance to clinical care as well as to the basic science of human psychophysiology. Non-invasive brain studies in man start to unveil the age-old puzzles of pain-illusion, hypnosis and placebo in pain modulation. The neurophysiological and neurohemodynamic brain measures of experimental pain can now largely satisfy the psychophysiologist's dream, unimaginable only a few years ago, of modelling the body-brain, brain-mind, mind-matter duality in an inter-linking 3-P triad: physics (stimulus energy); physiology (brain activities); and psyche (perception). For neuropsychophysiology greater challenges lie ahead: (a) how to integrate a cohesive theory of human pain in the brain; (b) what levels of analyses are necessary and sufficient; (c) what constitutes the structural organisation of the pain matrix; (d) what are the modes of processing among and across the sites of these structures; and (e) how can neural computation of these processes in the brain be carried out? We may envision that modular identification and delineation of the arousal-attention, emotion-motivation and perception-cognition neural networks of pain processing in the brain will also lead to deeper understanding of the human mind. Two foreseeable impacts on clinical sciences and basic theories from brain mapping/neuroimaging are the plausible central origin in persistent pain and integration of sensory-motor function in pain perception.
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PMID:New perspectives in EEG/MEG brain mapping and PET/fMRI neuroimaging of human pain. 1158 73

Insular and SII cortices have been consistently shown by PET, fMRI, EPs, and MEG techniques to be activated bilaterally by a nociceptive stimulation. The aim of the present study was to refer to, and to compare within a common stereotactic space, the nociceptive responses obtained in humans by (i) PET, (ii) fMRI, (iii) dipole modeling of scalp LEPs, and (iv) intracerebral recordings of LEPs. PET, fMRI, and scalp LEPs were obtained from normal subjects during thermal pain. Operculoinsular LEPs were obtained from 13 patients using deep brain electrodes implanted for presurgical evaluation of drug-resistant epilepsy. Whatever the technique, we obtained responses which were located bilaterally in the insular and SII cortices. In electrophysiological responses (LEPs) the SII insular contribution peaked between 150 and 250 ms poststimulus and corresponded to the earliest portions of the whole cerebral response. Group analysis of PET and fMRI data showed highly consistent responses contralateral to stimulation. On single-subject analysis, LEPs and fMRI activations were concentrated in relatively restricted volumes even though spatial sampling was quite different for both techniques. Despite our multimodal approach, however, it was not possible to separate insular from SII activities. Individual variations in the anatomy and function of SII and insular cortices may explain this limitation. This multimodal study provides, however, cross-validated spatial and temporal information on the pain-related processes occurring in the operculoinsular region, which thus appears as a major site for the early cortical pain encoding in the human brain.
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PMID:Role of operculoinsular cortices in human pain processing: converging evidence from PET, fMRI, dipole modeling, and intracerebral recordings of evoked potentials. 1241 73

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

Complex regional pain syndromes (CRPS, reflex sympathetic dystrophy, causalgia) are painful disorders that develop after trauma affecting a limb with (I) or without (II) nerve injury. Clinical features are pain, impairment of motor function, swelling and autonomic abnormalities (changes in sweating and blood flow). Autonomic abnormalities. The maximal skin temperature difference between the affected and unaffected extremity that occurs during a controlled thermoregulation can be used as a diagnostic tool. SMP. Sympathetic outflow to the painful extremity was experimentally activated. The intensity as well as area of spontaneous pain and mechanical hyperalgesia increased considerably in patients that had been classified as having SMP by positive sympathetic blocks. A pathological interaction between sympathetic vasoconstrictor and afferent neurons within the affected skin is the likely explanation for SMP in CRPS patients. Motor abnormalities. Kinematic analysis of target reaching as well as grip force analysis showed a pathological sensorimotor integration located in the parietal cortex. Furthermore, MEG studies demonstrated a continuous inhibition of the primary motor cortex. Neurogenic inflammation. Some features of acute CRPS (vasodilatation, swelling, pain) indicate a localized inflammatory process. Transcutaneous electrical stimulation of nociceptive C-fibre provoked protein extravasation into the interstitial fluid (microdialysis) only in CRPS patients and not in controls.
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PMID:Mechanistic and clinical aspects of complex regional pain syndrome (CRPS). 1546 53

The ability to localize both touch and pain has been attributed mainly to the primary somatosensory cortex (S1), based on its fine somatotopic mapping of tactile inputs. Recently, S1 has also been implicated in the differentiation of noxious stimulation, such as distinguishing between pain arising from viscera and skin. Recent MEG and fMRI studies show that there is at least a rudimentary tactile topographic representation in the supra-sylvian cortex [encompassing secondary somatosensory area (S2)], suggesting that this area may contribute to touch localization. Nevertheless, the role of this region in pain localization or its role in the differentiation of various types of pain has not been clearly established. Healthy subjects (four males, three females) underwent fMRI-scanning (1.5 T, standard head coil, BOLD analysis) during painful balloon distention of the distal esophagus and painful heat on the midline chest in the zone of referred pain for the esophageal stimulation. Five of the seven subjects exhibited significant activation of the parasylvian region in both experimental conditions, and in each of these five subjects activation related to esophageal pain was represented more laterally within the parasylvian cortex than that associated with cutaneous trunk pain (paired t-test, p's < 0.01). Our results suggest segregation of visceral esophageal and cutaneous chest afferents within parasylvian cortex, possibly implicating this region in the perceptual differentiation of visceral and cutaneous pain.
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PMID:Visceral and cutaneous pain representation in parasylvian cortex. 1590 31

Functional brain imaging of pain over the last years has provided insight into a distributed anatomical matrix involved in pain processing which includes multiple cortical areas. EEG/MEG-based imaging studies have mostly relied on settings of evoked nociception. We report here the spontaneous presence of enhanced activations in the pain matrix of the patient group on the basis of continuous EEG and functional Low Resolution Electromagnetic Tomography (LORETA) from 16 chronic neurogenic pain patients and 16 healthy controls. These overactivations occurred predominantly within the high theta (6-9 Hz) and low beta frequency ranges (12-16 Hz). Theta and beta overactivations were localized to multiple pain-associated areas, primarily to insular (IC), anterior cingulate (ACC), prefrontal, and inferior posterior parietal cortices, as well as to primary (S1), secondary (S2), and supplementary somatosensory (SSA) cortices. After a therapeutic lesion in the thalamus (central lateral thalamotomy, CLT), we followed a subgroup of 6 patients. Twelve months after surgery, activation in cingulate and insular cortices was significantly reduced. The presence of rhythmic processes in multiple, partially overlapping areas of the cortical pain matrix concur with the concept of thalamocortical dysrhythmia (TCD) that predicts increased thalamocortical low and high frequency oscillations ensuing from thalamic desactivation. These spontaneous, ongoing, frequency-specific overactivations may therefore serve as an anatomo-physiological hallmark of the processes underlying chronic neurogenic pain.
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PMID:Persistent EEG overactivation in the cortical pain matrix of neurogenic pain patients. 1652 93


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