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

Positron emission tomography studies have identified a common set of brain regions activated by pain. No studies, however, have quantitatively examined pain-induced CBF changes. To better characterize CBF during pain, 14 subjects received positron emission tomography scans during rest, during capsaicin-evoked pain (250 micrograms, intradermal injection), and during innocuous vibration. Using the H215O intravenous bolus method with arterial blood sampling, global CBF changes were assessed quantitatively. Painful stimulation produced a 22.8% decrease in global CBF from resting levels (P < 0.0005). This decrease was not accounted for by arterial PCO2 or heart rate changes. Although the exact mechanism remains to be determined, this pain-induced global decrease represents a previously unidentified response of CBF.
J Cereb Blood Flow Metab 1998 Feb
PMID:Global cerebral blood flow decreases during pain. 946 55

Primary headache syndromes, such as cluster headache and migraine, are widely described as vascular headaches, although considerable clinical evidence suggests that both are primarily driven from the brain. The shared anatomical and physiologic substrate for both of these clinical problems is the neural innervation of the cranial circulation. Functional imaging with positron emission tomography has shed light on the genesis of both syndromes, documenting activation in the midbrain and pons in migraine and in the hypothalamic gray in cluster headache. These areas are involved in the pain process in a permissive or triggering manner rather than as a response to first-division nociceptive pain impulses. In a positron emission tomography study in cluster headache, however, activation in the region of the major basal arteries was observed. This is likely to result from vasodilation of these vessels during the acute pain attack as opposed to the rest state in cluster headache, and represents the first convincing activation of neural vasodilator mechanisms in humans. The observation of vasodilation was also made in an experimental trigeminal pain study, which concluded that the observed dilation of these vessels in trigeminal pain is not inherent to a specific headache syndrome, but rather is a feature of the trigeminal neural innervation of the cranial circulation. Clinical and animal data suggest that the observed vasodilation is, in part, an effect of a trigeminoparasympathetic reflex. The data presented here review these developments in the physiology of the trigeminovascular system, which demand renewed consideration of the neural influences at work in many primary headaches and, thus, further consideration of the physiology of the neural innervation of the cranial circulation. We take the view that the known physiologic and pathophysiologic mechanisms of the systems involved dictate that these disorders should be collectively regarded as neurovascular headaches to emphasize the interaction between nerves and vessels, which is the underlying characteristic of these syndromes. Moreover, the syndromes can be understood only by a detailed study of the cerebrovascular physiologic mechanisms that underpin their expression.
J Cereb Blood Flow Metab 1999 Feb
PMID:The trigeminovascular system in humans: pathophysiologic implications for primary headache syndromes of the neural influences on the cerebral circulation. 1002 65

The binding of [11C]diprenorphine to mu, kappa, and delta subsites in cortical and subcortical structures was measured by positron emission tomography in vivo in six patients before and after surgical relief of trigeminal neuralgia pain. The volume of distribution of [11C]diprenorphine binding was significantly increased after thermocoagulation of the relevant trigeminal division in the following areas: prefrontal, insular, perigenual, mid-cingulate and inferior parietal cortices, basal ganglia, and thalamus bilaterally. In addition to the pain relief associated with the surgical procedure, there also was an improvement in anxiety and depression scores. In the context of other studies, these changes in binding most likely resulted from the change in the pain state. The results suggest an increased occupancy by endogenous opioid peptides during trigeminal pain but cannot exclude coexistent down-regulation of binding sites.
J Cereb Blood Flow Metab 1999 Jul
PMID:Measurement of changes in opioid receptor binding in vivo during trigeminal neuralgic pain using [11C] diprenorphine and positron emission tomography. 1041 36

For much of the twentieth century migraine and cluster headache have been considered as vascular headaches whose pathophysiology was determined by changes in cranial vascular diameter. To examine nociceptive neural influences on the cranial circulation, the authors studied healthy volunteers' responses to injection of the pain-producing compound capsaicin in terms of the caliber of the internal carotid artery. The study was conducted using magnetic resonance angiographic techniques. Injection of capsaicin into the skin innervated by the ophthalmic (first) division of the trigeminal nerve elicited 40% +/- 27% (mean +/- SD) increase in vascular cross-sectional area in the right (ipsilateral) internal carotid artery when compared with the mean baseline ( P < 0.001). Injection of capsaicin into the skin of the chin to stimulate the mandibular (third) division of the trigeminal nerve and into the leg led to a similar pain perception and failed to produce any significant change in vessel caliber. The data suggest that there is a highly functionally organized, somatotopically congruent trigeminal innervation of the cranial vessels, with a potent vasodilator effect of the ophthalmic division on the large intracranial vessels. The data are consistent with the notion that pain drives changes in vessel caliber in migraine and cluster headache, not vice versa. These conditions therefore should be regarded as primary neurovascular headaches not as vascular headaches.
J Cereb Blood Flow Metab 2001 Oct
PMID:Magnetic resonance angiography in facial and other pain: neurovascular mechanisms of trigeminal sensation. 1159 94

We studied painful and non-painful somaesthetic sensations elicited by direct electrical stimulations of the insular cortex performed in 43 patients with drug refractory temporal lobe epilepsy, using stereotactically implanted depth electrodes. Painful sensations were evoked in the upper posterior part of the insular cortex in 14 patients, mostly in the right hemisphere. Non-painful sensations were elicited in the posterior part of the insular cortex in 16 patients, in both hemispheres. Thus, painful and non-painful somaesthetic representations in the human insula overlap. Both types of responses showed a trend toward a somatotopic organization. These results agree with previous anatomical and unit recording studies in monkeys indicating a participation of the posterior part of the insular cortex in processing both noxious and innocuous somaesthetic stimuli. In humans, both a posterior and an anterior pain-related cortical area have been described within the insular cortex using functional imaging. Our results help to define the respective functional roles of these two insular areas. Finally, lateralization in the right hemisphere of sites where painful sensations were evoked is coherent with the hypothesis of a preponderant role of this hemisphere in species survival.
Cereb Cortex 2002 Apr
PMID:Representation of pain and somatic sensation in the human insula: a study of responses to direct electrical cortical stimulation. 1188 53

The patterns of cortical activation evoked by tactile and mechanical painful stimulation in six normal subjects and three patients with complete resection of the corpus callosum are described and compared, with emphasis on the parietal operculum. Stimulus-related cortical activation was investigated by functional magnetic resonance imaging. In both groups, painful stimulation activated the first somatosensory, insular and cingulate cortices in the contralateral hemisphere, and the parietal opercular cortex in both hemispheres. Comparison between the two patterns of cortical activation demonstrated that ipsilateral activation by unilateral painful stimulation is at least partially independent of the corpus callosum and suggests a different organization of the pain and touch systems.
Cereb Cortex 2002 Apr
PMID:Mechanical noxious stimuli cause bilateral activation of parietal operculum in callosotomized subjects. 1188 59

The cortical areas that represent affectively positive and negative aspects of touch were investigated using functional magnetic resonance imaging (fMRI) by comparing activations produced by pleasant touch, painful touch produced by a stylus, and neutral touch, to the left hand. It was found that regions of the orbitofrontal cortex were activated more by pleasant touch and by painful stimuli than by neutral touch and that different areas of the orbitofrontal cortex were activated by the pleasant and painful touches. The orbitofrontal cortex activation was related to the affective aspects of the touch, in that the somatosensory cortex (SI) was less activated by the pleasant and painful stimuli than by the neutral stimuli. This dissociation was highly significant for both the pleasant touch (P < 0.006) and for the painful stimulus (P < 0.02). Further, it was found that a rostral part of the anterior cingulate cortex was activated by the pleasant stimulus and that a more posterior and dorsal part was activated by the painful stimulus. Regions of the somatosensory cortex, including SI and part of SII in the mid-insula, were activated more by the neutral touch than by the pleasant and painful stimuli. Part of the posterior insula was activated only in the pain condition and different parts of the brainstem, including the central grey, were activated in the pain, pleasant and neutral touch conditions. The results provide evidence that different areas of the human orbitofrontal cortex are involved in representing both pleasant touch and pain, and that dissociable parts of the cingulate cortex are involved in representing pleasant touch and pain.
Cereb Cortex 2003 Mar
PMID:Representations of pleasant and painful touch in the human orbitofrontal and cingulate cortices. 1257 Nov 20

The ability to locate pain plays a pivotal role in immediate defence and withdrawal behaviour. However, it is unclear to what extent nociceptive information is relayed to and processed in subcortical structures relevant for motor preparation and possibly the generation of withdrawal behaviour. We used single-trial functional magnetic resonance imaging (fMRI) to assess whether nociceptive information is represented in the putamen in a somatotopic manner. We therefore applied thulium-YAG laser-evoked pain stimuli, which had no concomitant tactile component, to the dorsum of the left hand and foot to 15 healthy subjects in a randomized order. In addition, 11 subjects were stimulated on the right body side. Differential representations of hand- and foot-related blood oxygen level dependent (BOLD) responses within the putamen were assessed using a single subject approach. Nociceptive stimuli significantly activated the putamen bilaterally. However, a somatotopic organization for hand- and foot-related responses was only present in the contralateral putamen. Here the foot was located anteriorly and medially to the hand, which parallels results from anatomical and microstimulation studies in monkeys and also human imaging data on the arrangement of movement related activity in the putamen. This result provides evidence for the hypothesis that behaviourally relevant nociceptive information without additional information from the tactile system is represented in the putamen and made available for pain related motor responses.
Cereb Cortex 2004 Dec
PMID:Somatotopic representation of nociceptive information in the putamen: an event-related fMRI study. 1521 95

The mechanisms by which vibrotactile stimuli relieve pain are not well understood, especially in humans. We recorded cortical magnetic responses to paired noxious (intra-epidermal electrical stimulation, IES) and innocuous (transcutaneous electrical stimulation, TS) stimuli applied to the back at a conditioning-test interval (CTI) of -500 to 500 ms. Results showed that IES-induced responses were remarkably attenuated when TS was applied 20-60 ms later and 0-500 ms earlier than IES (CTI = -60 to 500 ms). Since the signals evoked by IES reached the spinal cord (CTI = -60 to -20 ms conditions) and the cortex (-60 and -40 ms condition) earlier than those evoked by TS, the present results indicate that cortical responses to noxious stimuli can be inhibited by innocuous tactile stimuli at the cortical level, with minimal contribution at the spinal level.
Cereb Cortex 2006 Mar
PMID:Temporal analysis of cortical mechanisms for pain relief by tactile stimuli in humans. 1590 50

The neuronal activity of the resting human brain is dominated by spontaneous oscillatory activity of primary visual, somatosensory and motor areas. These spontaneous brain rhythms are related to the functional state of a system. A higher amplitude of oscillatory activity is thought to reflect an idling state, whereas a lower amplitude is associated with activation and higher excitability of the specific system. Here, we used magnetoencephalography to investigate the effects of pain on spontaneous brain rhythms. Our results show that a focally applied brief painful stimulus globally suppresses spontaneous oscillations in somatosensory, motor and visual areas. This global suppression contrasts with the regionally specific suppressions of other modalities and shows that pain induces a widespread change in cortical function and excitability. This global change in excitability may reflect the alerting function of pain which opens the gates for processing of and reacting to stimuli of existential relevance.
Cereb Cortex 2006 Apr
PMID:Pain suppresses spontaneous brain rhythms. 1603 27


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