Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0184567 (acute pain)
 3,962 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was undertaken to explore whether the neural substrates demonstrated in brain imaging studies on experimentally induced pain are involved in the perception of chronic neuropathic pain. We investigated the cerebral representation of chronic lateralised ongoing pain in patients with painful mononeuropathy (PMN, i.e., pain in the distribution of a nerve, neuralgia) with positron emission tomography (PET), using regional cerebral blood flow (rCBF) as an index for neuronal activity. Eight patients (29-53 years) with PMN in the lower extremity (4 in the right, 4 in the left) were recruited. Paired comparisons of rCBF were made between the patient's habitual pain (HP) state and the pain alleviated (PA) state following a successful regional nerve block (RNB) with lidocaine. The ongoing neuropathic pain resulted in activation of bilateral anterior insula, posterior parietal, lateral inferior prefrontal, and posterior cingulate cortices as well as the posterior sector of the right anterior cingulate cortex (ACC), Brodmann area (BA) 24, regardless of the side of PMN. In addition, a reduction in rCBF was noted in the contralateral posterior thalamus. No significant change of rCBF was detected in the somatosensory areas, i.e., SI and SII. The cerebral activation pattern, while addressing the differences between the HP and PA states, emphasises the affective-motivational dimension in chronic ongoing neuropathic pain. The striking preferential activation of the right ACC (BA 24), regardless of the side of the PMN, not only confirms that the ACC participates in the sensorial/affectional aspect of the pain experience but also suggests a possible right hemispheric lateralisation of the ACC for affective processing in chronic ongoing neuropathic pain. Our data suggests that the brain employs different central mechanisms for chronic neuropathic pain and experimentally induced acute pain, respectively.
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PMID:Central representation of chronic ongoing neuropathic pain studied by positron emission tomography. 862 89

The study of pain integration, in vivo, within the human brain has been largely improved by the functional neuro-imaging techniques available for about 10 years. Positron Emission Tomography (PET), complemented by laser evoked potentials (LEP) and functional Magnetic Resonance Imaging (fMRI) can nowadays generate maps of physiological or neuropathic pain-related brain activity. LEP and fMRI complement PET by their better temporal resolution and the possibility of individual subject analyze. Recent advances in our knowledge of pain mechanisms concern physiological acute pain, neuropathic pain and investigation of analgesic mechanisms. The sixteen studies using PET have demonstrated pain-related activations in thalamus, insula/SII, anterior cingulate and posterior parietal cortices Activity in right pre-frontal and posterior parietal cortices, anterior cingulate and thalami can be modulated by attention (hypnosis, chronic pain, diversion, selective attention to pain) and probably subserve attentional processes rather than pain analysis. Responses in insula/SII cortex presumably subserve discriminative aspects of pain perception while SI cortex is particularly involved in particular aspects of pain discrimination (movement, contact.) In patients, neuropathic pain, angina and atypical facial pain result in PET abnormalities whose significance remain obscure but which are localized in thalamus and anterior cingulate cortices suggesting their distribution is not random while discriminative responses remain detectable in insula/SII. Drug or stimulation induced analgesia are associated with normalization of basal thalamic abnormalities associated with many chronic pains. The need to investigate the significance of these responses, their neuro-chemical correlates (PET), their time course, the individual strategies by which they have been generated by correlating PET data with LEP and fMRI results, are the challenges that remain to be addressed in the next few years by physicians and researchers. To advance our knowledge of the mechanisms generating both abnormal pain and analgesia (drugs and surgical techniques) in patients is the main motivation of such anexciting challenge.
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PMID:[Positron emission tomography to study central pain integration]. 1079 10

Brain responses to pain, assessed through positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) are reviewed. Functional activation of brain regions are thought to be reflected by increases in the regional cerebral blood flow (rCBF) in PET studies, and in the blood oxygen level dependent (BOLD) signal in fMRI. rCBF increases to noxious stimuli are almost constantly observed in second somatic (SII) and insular regions, and in the anterior cingulate cortex (ACC), and with slightly less consistency in the contralateral thalamus and the primary somatic area (SI). Activation of the lateral thalamus, SI, SII and insula are thought to be related to the sensory-discriminative aspects of pain processing. SI is activated in roughly half of the studies, and the probability of obtaining SI activation appears related to the total amount of body surface stimulated (spatial summation) and probably also by temporal summation and attention to the stimulus. In a number of studies, the thalamic response was bilateral, probably reflecting generalised arousal in reaction to pain. ACC does not seem to be involved in coding stimulus intensity or location but appears to participate in both the affective and attentional concomitants of pain sensation, as well as in response selection. ACC subdivisions activated by painful stimuli partially overlap those activated in orienting and target detection tasks, but are distinct from those activated in tests involving sustained attention (Stroop, etc.). In addition to ACC, increased blood flow in the posterior parietal and prefrontal cortices is thought to reflect attentional and memory networks activated by noxious stimulation. Less noted but frequent activation concerns motor-related areas such as the striatum, cerebellum and supplementary motor area, as well as regions involved in pain control such as the periaqueductal grey. In patients, chronic spontaneous pain is associated with decreased resting rCBF in contralateral thalamus, which may be reverted by analgesic procedures. Abnormal pain evoked by innocuous stimuli (allodynia) has been associated with amplification of the thalamic, insular and SII responses, concomitant to a paradoxical CBF decrease in ACC. It is argued that imaging studies of allodynia should be encouraged in order to understand central reorganisations leading to abnormal cortical pain processing. A number of brain areas activated by acute pain, particularly the thalamus and anterior cingulate, also show increases in rCBF during analgesic procedures. Taken together, these data suggest that hemodynamic responses to pain reflect simultaneously the sensory, cognitive and affective dimensions of pain, and that the same structure may both respond to pain and participate in pain control. The precise biochemical nature of these mechanisms remains to be investigated.
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PMID:Functional imaging of brain responses to pain. A review and meta-analysis (2000). 1112 40

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.
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PMID:Single subject pharmacological-MRI (phMRI) study: modulation of brain activity of psoriatic arthritis pain by cyclooxygenase-2 inhibitor. 1626 29

Functional brain imaging techniques allow to noninvasively visualize neuronal activity and associated metabolic consequences. In combination with elegant experimental paradigms in both healthy volunteers and, increasingly, in patients, functional brain imaging has led to a vast accumulation of knowledge concerning the CNS mechanisms involved in pain perception and pain modulation in humans. The so-called "pain matrix" represents a dynamic network of cortical and subcortical brain regions regularly activated by acute pain. This includes the somatosensory cortices (SI, SII), insular cortex, the cingulate cortex, prefrontal areas, amygdala, thalamus, brainstem and cerebellum. The subjective perception of pain is substantially influenced by context-dependent intracortical modulations and the descending pain modulatory system. This system includes cingulo-frontal brain areas together with specific brainstem nuclei that can exert control over nociceptive input at the level of the dorsal horn of the spinal cord. Recent studies support the view that a dysfunctional interaction between the ascending and descending pain system may contribute to the development or maintenance of chronic pain states. Here we provide an overview of the principles, applications, key findings and recent advances of functional imaging in pain research.
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PMID:[Functional imaging in pain research]. 2067 99

The visual context of seeing the body can reduce the experience of acute pain, producing a multisensory analgesia. Here we investigated the neural correlates of this "visually induced analgesia" using fMRI. We induced acute pain with an infrared laser while human participants looked either at their stimulated right hand or at another object. Behavioral results confirmed the expected analgesic effect of seeing the body, while fMRI results revealed an associated reduction of laser-induced activity in ipsilateral primary somatosensory cortex (SI) and contralateral operculoinsular cortex during the visual context of seeing the body. We further identified two known cortical networks activated by sensory stimulation: (1) a set of brain areas consistently activated by painful stimuli (the so-called "pain matrix"), and (2) an extensive set of posterior brain areas activated by the visual perception of the body ("visual body network"). Connectivity analyses via psychophysiological interactions revealed that the visual context of seeing the body increased effective connectivity (i.e., functional coupling) between posterior parietal nodes of the visual body network and the purported pain matrix. Increased connectivity with these posterior parietal nodes was seen for several pain-related regions, including somatosensory area SII, anterior and posterior insula, and anterior cingulate cortex. These findings suggest that visually induced analgesia does not involve an overall reduction of the cortical response elicited by laser stimulation, but is consequent to the interplay between the brain's pain network and a posterior network for body perception, resulting in modulation of the experience of pain.
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PMID:Linking pain and the body: neural correlates of visually induced analgesia. 2235 44

Anterior midcingulate cortex (aMCC) has been shown to be involved in most of the functional imaging studies investigating acute pain. For 10-15 years, it has even been a main focus of interest for pain studies, considering that neurons in the aMCC could encode for pain intensity. This latter function is now presumed to occur in secondary somatosensory (SII) area and/or insular cortices, while anterior cingulate cortex (ACC) is supposed to sustain other functions such as pain-related attention, arousal, motor withdrawal reflex, pain modulations, and engagement of endogenous pain control system. The quantitative imaging studies have shown a rich density of opioid receptors in the ACC. Thus, the perigenual subdivision has been suggested to participate in top-down controls of pain, (including the placebo effects known to be opioid mediated), mainly (but not exclusively) through the connection between the orbitofrontal/subgenual ACC and the periaqueductal gray (PAG). From this rationale, this area may lead to neurosurgical targeting including electrical stimulation for intractable pain in the future. A number of imaging studies have also reported activity changes in the posterior cingulate cortex during pain and proposed its speculative involvement to modulate the conscious experience of pain according to elements from the context and awareness of the self and others.
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PMID:Cingulate-mediated approaches to treating chronic pain. 3173 19