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

Several imaging modalities are available for evaluating the patient with acute scrotal pain. Until recently, scintigraphy was the initial procedure of choice in most patients, as it was the only noninvasive technique for determining integrity of blood flow to the testicle. Ultrasound was valuable when the scintiscan was inconclusive or in the setting of scrotal trauma. With the advent of color Doppler sonography, information about both structure and blood flow can be obtained by means of a single imaging study. If initial promising results with this newer technique are borne out, color Doppler is likely to become the primary diagnostic test in patients with acute scrotal pain. The role of MRI and MRS has yet to be defined.
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PMID:Acute diseases of the scrotum. 186 74

We have used 31phosphorus magnetic resonance spectroscopy (31P-MRS) to study foot muscle metabolism in patients with peripheral vascular disease. Sixteen patients with calf claudication, 32 patients with rest pain and 13 control subjects had spectra collected from the foot muscle, Extensor digitorum brevis, ankle pressures measured and, in most cases, transcutaneous O2 and CO2 recordings made over the foot. The intracellular pH and the ratio of inorganic phosphate to phosphocreatine (Pi/PCr) obtained from the MR spectra were significantly higher (p less than 0.005 and p less than 0.02, respectively) in the muscle of patients with rest pain and were particularly high in those with gangrene or ulceration. Ankle pressures and transcutaneous O2 and CO2 measurements failed to distinguish those patients with advanced peripheral ischaemia. These results suggest that MRS measurements of metabolic changes in foot muscle are useful in the detection and quantitation of significant distal ischaemia.
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PMID:Muscle ischaemia in peripheral vascular disease studied by 31P-magnetic resonance spectroscopy. 227 75

Three patients (two of them siblings) presented with easy fatiguability and prominent postexercise pain. Muscle biopsy showed that large areas of about one third of the type II fibers were completely devoid of mitochondria. The remaining mitochondria were unusually large in size, but otherwise normal ultrastructurally. In two patients, 31P in vivo MRS showed low phosphocreatine (PCr), high ADP, low phosphorylation potential at rest and slow ADP and PCr recovery after aerobic exercise. This appears to be a pathologically unique form of metabolic myopathy. The cause of the focal mitochondrial depletion is not known. It should be distinguished from the mtDNA depletion syndrome in which muscle mitochondria are not reduced, but proliferate.
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PMID:Familial myopathy with conspicuous depletion of mitochondria in muscle fibers: a morphologically distinct disease. 776 93

Research into migraine pathophysiology has been hampered by the episodic nature and unpredictable onset of migraine attacks. Recently, newer imaging techniques have been providing noninvasive methods of studying metabolism and hemodynamics in the brains of migraineurs during and between acute attacks. 133Xe blood flow techniques, transcranial Doppler, and SPECT have all been employed to investigate hemodynamic changes during migraine aura. PET has been useful in the study of migraine without aura, with findings of increased blood flow related to pain in cortical areas and in the medial brainstem. Currently, three functional MRI imaging techniques are being used in migraine research. Diffusion-weighted imaging has shown normal findings in measures of the ability of neurons to maintain osmotic gradients. Studies using perfusion-weighted imaging have shown alterations in relative cerebral blood flow (CBF), relative cerebral blood volume, and mean transit time during migraine visual aura. The blood oxygen level-dependent technique can supply information related to neuronal activation during acute migraine aura. MRS has been used with mixed success to look for evidence of abnormal energy metabolism in the brains of migraineurs. Magnetoencephalography studies support the presence of a spreading depression-like phenomenon in migraine with aura. Two groups have used transcranial magnetic stimulation to assess whether neurons in the occipital cortex are hyperexcitable, predisposing patients to develop aura symptoms. Despite conflicting findings, migraine with visual aura appears to be generally associated with transient decreases in regional CBF.
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PMID:Functional neuroimaging: enhanced understanding of migraine pathophysiology. 1108 18

The neurobiology of chronic pain, including chronic back pain, is unknown. Structural imaging studies of the spine cannot explain all cases of chronic back pain. Functional brain imaging studies indicate that the brain activation patterns are different between chronic pain patients and normal subjects, and the thalamus, and prefrontal and cingulate cortices are involved in some types of chronic pain. Animal models of chronic pain suggest abnormal spinal cord chemistry. Does chronic pain cause brain chemistry changes? We examined brain chemistry changes in patients with chronic back pain using in vivo single- voxel proton magnetic resonance spectroscopy ((1)H-MRS). In vivo (1)H-MRS was used to measure relative concentrations of N-acetyl aspartate, creatine, choline, glutamate, glutamine, gamma-aminobutyric acid, inositol, glucose and lactate in relation to the concentration of creatine. These measurements were performed in six brain regions of nine chronic low back pain patients and 11 normal volunteers. All chronic back pain subjects underwent clinical evaluation and perceptual measures of pain and anxiety. We show that chronic back pain alters the human brain chemistry. Reductions of N-acetyl aspartate and glucose were demonstrated in the dorsolateral prefrontal cortex. Cingulate, sensorimotor, and other brain regions showed no chemical concentration differences. In chronic back pain, the interrelationship between chemicals within and across brain regions was abnormal, and there was a specific relationship between regional chemicals and perceptual measures of pain and anxiety. These findings provide direct evidence of abnormal brain chemistry in chronic back pain, which may be useful in diagnosis and future development of more effective pharmacological treatments.
Pain 2000 Dec 15
PMID:Abnormal brain chemistry in chronic back pain: an in vivo proton magnetic resonance spectroscopy study. 1111 88

In our previous in vivo proton magnetic resonance spectroscopy ((1)H MRS) study we found reduced levels of N-acetylaspartate in dorsolateral prefrontal cortex of chronic back pain patients. This study tests whether these chemical abnormalities can be detected in other pain states. Using (1)H MRS, we measured levels for N-acetylaspartate and other identifiable chemicals relative to creatine in four bilateral brain regions, including dorsolateral prefrontal cortex, orbitofrontal cortex, cingulate, and thalamus, in a case of intractable severe sympathetically mediated chronic pain [complex regional pain syndrome (CRPS) type I]. The subject's chemical variations in the brain were compared to the same regional chemicals in 10 normal subjects (age- and sex-matched). Univariate statistics showed reduced levels of N-acetylaspartate in bilateral dorsolateral prefrontal cortex and increased levels of myo-inositol in left orbitofrontal cortex of the patient with intractable severe CRPS type I. These data support our original hypothesis that depletion of N-acetylaspartate in dorsolateral prefrontal cortex is a chemical marker of chronic pain, indicating for neuronal degeneration. Unpredicted changes of orbitofrontal myo-inositol may be related to the specific mood/affective state in an extreme pain perception. This is the first report, which identifies chemical markers in the prefrontal cortex for objective measurement and monitoring of CRPS type I. This information might lead to valuable insights into diagnosis and future effective interventions of CRPS type I (e.g., prefrontal brain stimulation).
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PMID:Decreased levels of N-acetylaspartate in dorsolateral prefrontal cortex in a case of intractable severe sympathetically mediated chronic pain (complex regional pain syndrome, type I). 1202 96

The neurobiology of the interaction between pain and anxiety is unknown. The present study examined interrelationships between: regional brain chemistry (as identified by in vivo proton magnetic resonance spectroscopy [(1)H-MRS] in dorsolateral prefrontal cortex [DLPFC], orbitofrontal cortex [OFC], cingulate and thalamus), pain (as measured by short form of the McGill Pain Questionnaire [SF-MPQ]), and anxiety (measured by the State-Trait Anxiety Inventory) in chronic low back pain (CLBP) patients, and contrasted to the relationship between brain chemistry and anxiety in sex and age-matched normal subjects. The results show that brain chemistry depends on a 3-way interaction of brain regions examined, subject groups (normal vs. CLBP), and anxiety levels (high vs. low). The concentration of N-Acetyl aspartate (the largest peak in (1)H-MRS) in OFC could distinguish between anxiety levels and between subject groups. Chemical-perceptual relationships were analyzed by calculating correlations between regional chemicals and perceptual measures of pain and anxiety. To isolate pain from anxiety, these maps were subdivided based on anxiety and, in the CLBP patients along anxiety-more-related vs. anxiety-less-related pain descriptors and along sensory vs. affective pain descriptors. There was a precise relationship between perception and brain chemistry. The chemical-perceptual network best related to pain in CLBP patients was comprised of the DLPFC and OFC; the chemical-anxiety network was best related to the OFC chemistry in normals and to all four regions studied in CLBP patients; and the cingulate was best related to the affective component of pain. We conclude that the chemical-perceptual mapping differentiates between closely related perceptual states of pain and anxiety in chronic pain and provides a brain regional-chemical-perceptual description of the long-term reorganization that occurs with chronic pain.
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PMID:Brain chemistry reflects dual states of pain and anxiety in chronic low back pain. 1237 63

Receptors for ATP in the peripheral nervous system may contribute to the transduction of sensory, including nociceptive, stimuli and are candidates in the pathogenesis of neuropathic pain. In a complex neural tissue, such as the human peripheral nerve trunk, ATP may activate P2X, P2Y, and adenosine receptors present on various cell types. Experiments were performed on segments of isolated human sural nerves. The experimental set-up enabled simultaneous recording of C fiber excitability, intracellular Ca(2+) ([Ca(2+)](i)) and extracellular K(+) activity (aK(e)). The increase in excitability of unmyelinated fibers seen during bath application of both ATP and adenosine was reversed to a reduction in axonal excitability in the presence of 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolol[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol (ZM 241385), an antagonist of adenosine A2 receptors. The pharmacological profile of the axonal subexcitability indicates the presence and activation of adenosine A1 receptors. Intracellular Ca(2+) transients were observed during bath application of ATP but not of adenosine and were blocked by 2'-deoxy- N(6)-methyladenosine 3',5'-bisphosphate (MRS 2179), an antagonist at P2Y(1) receptors. K(+)-sensitive microelectrodes were used to search for a possible activation of P2X receptors by ATP. In isolated rat vagus nerve, activation of P2X receptors by alpha,beta-methylene-adenosine 5'-triphosphate (alpha,beta-meATP) and by diadenosine pentaphosphate (Ap5A) resulted in a rapid, transient rise in the extracellular K(+) activity. In contrast, in human nerve, application of P2X receptor agonists did not result in a detectable elevation of aK(e). The data suggest that ATP-induced changes in axonal excitability and of [Ca(2+)](i) result from activation of adenosine A2, A1 and P2Y nucleotide receptors in human nerve; a contribution of P2X receptors was not found with the methods used. It is suggested that antagonists of A2 receptors might suppress enhanced activity in human nociceptive afferent nerve fibers under conditions in which ATP and/or adenosine is released into the trunk of a human peripheral nerve.
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PMID:Activation of adenosine and P2Y receptors by ATP in human peripheral nerve. 1238 74

1. The potential neuroprotective actions of the A3 adenosine receptor (A3AR) were investigated using mice with functional deletions of the A3AR (A3AR-/-) in behavioral assessments of analgesia, locomotion, tests predictive of depression and anxiety, and the effects of mild hypoxia on cognition and neuronal survival. 2. Untreated A3AR-/- mice were tested in standard behavioral paradigms, including activity in the open field, performance in the hot-plate, tail-flick, tail-suspension, and swim tests, and in the elevated plus maze. In addition, mice were exposed repeatedly to a hypoxic environment containing carbon monoxide (CO). The cognitive effects of this treatment were assessed using the contextual fear conditioning test. After testing, the density of pyramidal neurons in the CA1, 2, and 3 subfields of the hippocampus was determined using standard histological and morphometric techniques. 3. A3AR-/- mice showed increased locomotion in the open field test, elevated plus maze (number of arm entries) and light/dark box (number of transitions). However, they spent more time immobile in two different tests of antidepressant activity (Swim and tail suspension tests). A3AR-/- mice also showed evidence of decreased nociception in the hotplate, but not tail-flick tests. Further, A3AR-/- mice were more vulnerable to hippocampal pyramidal neuron damage following episodes of carbon monoxide (CO)-induced hypoxia. One week after exposure to CO a moderate loss of pyramidal neurons was observed in all hippocampal subfields of both wild-type (A3AR+/+) and A3AR-/- mice. However, the extent of neuronal death in the CA2-3 subfields was less pronounced in A3AR+/+ than A3AR-/- mice. This neuronal loss was accompanied by a decline in cognitive function as determined using contextual fear conditioning. These histological and cognitive changes were reproduced in wild-type mice by repeatedly administering the A3AR-selective antagonist MRS 1523 (5-propyl-2-ethyl-4-propyl-3-(ethylsulfanylcarbonyl)-6-phenylpyridine-5-carboxylate 1 mg/kg i.p.). 4. These results indicate that pharmacologic or genetic suppression of A3AR function enhances some aspects of motor function and suppresses pain processing at supraspinal levels, while acting as a depressant in tests predictive of antidepressant action. Consistent with previous reports of the neuroprotective actions of A3AR agonists, A3AR-/- mice show an increase in neurodegeneration in response to repeated episodes of hypoxia.
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PMID:Behavioral characterization of mice lacking the A3 adenosine receptor: sensitivity to hypoxic neurodegeneration. 1282 37

Glutamate, a major excitatory neurotransmitter, has been implicated as an important mediator in the neurotransmission, potentiation, and negative affect associated with pain. We present results showing that a painful stimulus elicits a dynamic increase in glutamate (9.3% from baseline) concentrations in the anterior cingulate cortex, detectable using proton Magnetic Resonance Spectroscopy ((1)H-MRS). Increases in glutamine levels were also seen, which correlate strongly with the subjective level of pain experienced by participants (r(2) = 0.58, P < 0.01). These novel findings are the first time a dynamic change in glutamate and glutamine levels from baseline in response to an external stimuli has been measured in a single proton MRS scanning session. As such, this report demonstrates the efficacy of (1)H-MRS as a non-invasive tool for the study of neural responses to pain in vivo. The paradigm used in this study demonstrates that dynamic glutamate/glutamine changes due to stimulation are measurable by proton MRS, and could provide a means of testing novel pharmaceutical agents and other treatments for chronic pain.
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PMID:A novel technique to study the brain's response to pain: proton magnetic resonance spectroscopy. 1590 22


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