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

Groups of 27 inpatients with moderate or severe postoperative, fracture, or somatic pain were given single oral doses of propoxyphene napsylate (P), fenoprofen calcium (F), combinations of P and F, aspirin, or placebo. The increasing rank order for effectiveness, with doses in milligrams, was placebo, P50, aspirin 650, F600, F50, P50 + F50, F200, P50 + F600, P50 + F200, P200 + F50, P200, P200 + F200, and P200 + F600. The overall analgesic response to propoxyphene in this dose range (50 to 200 mg) increased linearly with increasing doses. The fenoprofen response also increased in proportion to the dose up to 200 mg; the overall response to 600 mg was not significantly different from that to 200 mg. Propoxyphene napsylate and fenoprofen calcium had additive analgesic effects. There were no drug-related adverse reports.
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PMID:A comparative analgesic study of propoxyphene, fenoprofen, the combination of propoxyphene and fenoprofen, aspirin, and placebo. 36 51

The objective of this work was to simultaneously measure pain-related spinal and supraspinal physiological responses in humans. The sural nerve compound action potential (CAP), the spinal withdrawal reflex (RIII), the somatosensory evoked potential (SEP) and subjective magnitude ratings were elicited by electrical stimulation of the sural nerve in 10 healthy subjects. The sural nerve CAP was used to normalize the evoking stimulus current and to help identify the peripheral nerve afferent types contributing to the physiological and psychophysical responses. Normalizing stimulus current to a proportion of that which elicited a just maximal sural nerve CAP significantly reduced individual variability in magnitude ratings, the RIII and the SEP. Pain and RIII responses only occurred at stimulus levels that were greater than or equal to 1.5 x that which produced a just maximal sural nerve CAP and both responses were positively related to stimulus intensity above that level. Activity in the large diameter A beta fibers will be saturated at stimulus levels near that which produced a just maximal CAP, which implies that both the pain and RIII responses can be attributed to recruitment of the smaller diameter A delta fibers. Although the amplitudes of the P200 and P300 peaks of the SEP were significantly related to stimulation at noxious levels, both were also affected by stimulation at innocuous levels. This result implies that these peaks receive contributions from both noxious and innocuous somatosensory processes. Clearly, the non-pain-related components of these SEP peaks must be identified and isolated before their potential in measuring supraspinal nociceptive processes can be fully realized.
Pain 1991 Jun
PMID:Spinal and supraspinal correlates of nociception in man. 187 36

In order to determine the effects of attention and distraction on painful and non-painful stimuli, the amplitude changes of 3 components (N150, P200, P300) of the somatosensory event-related potential (SERP) elicited by painful and non-painful electrical stimuli were investigated. Painful and non-painful stimuli were determined using a visual analog scale. SERPs were recorded from 16 healthy volunteers at 5 midline and 4 left and 4 right hemispheric sites. The differences between the amplitudes of attended and ignored stimuli were quantified with a baseline-to-peak measure. ANOVA results revealed no significant attention or stimulus intensity effects for N150 but highly significant differences in P200 and P300 amplitudes between attended and ignored stimuli. In addition, P200 and P300 amplitudes were larger for strong stimuli than for weak stimuli, with no significant differences between non-painful and painful stimuli. These findings are consistent with the existence of a relative, rather than an absolute, relationship between SERP component amplitudes and subjective pain reports. Furthermore, the data give evidence that attentional manipulations represent a powerful method to decrease the perception of pain and that, when used with subjective and behavioral measures, the SERP represents a valuable asset in the multidimensional approach to pain measurement and assessment.
Pain 1989 Sep
PMID:Somatosensory event-related potentials to painful and non-painful stimuli: effects of attention. 281 41

Thermal (laser) evoked responses were obtained from 13 male volunteers. A single trial analysis technique with a latency adjusting adaptive filter was used to analyze evoked response amplitudes. Significant and substantial within-subject linear correlations were found between the magnitude (A) of the primary waveform (RMS muV of the P200--N300-P400 complex ) and subjective pain response (R) as well as stimulus intensity (S). Since subjective pain response was strongly correlated with stimulus intensity, the partial correlation coefficients were calculated for R vs. A with S controlled, and S vs. A with R controlled, for each subject. The partial correlations revealed a much stronger relationship between subjective response and the evoked response amplitude, suggesting that the primary complex may measure neural events in the pain perception process rather than transduction and transmission of the stimulus event.
Pain 1980 Feb
PMID:Single trial analysis of evoked potentials to noxious thermal stimulation in man. 736 35

Classical conditioning is involved in the acquisition of chronic pain. The present study investigated whether experimental pain responses can be conditioned using auditory stimuli in a differential trace conditioning paradigm. 16 healthy subjects served as paid volunteers. The UCS was an intracutaneous electrical stimulus applied to the left middle-finger (10 ms duration). Tones of 1000 and 1400 Hz (both 80 dB SPL, 50 ms) were used as CS+ and CS-, respectively. A trace conditioning paradigm was used with an 800 ms interval between CS and UCS. Somatosensory event related potentials (SEP) and auditory event related potentials (AEP) were recorded from 29 electrode sites. Subjective pain reports were measured with an adjective list that allowed a detailed description of subjects' sensations elicited by painful and auditory stimuli. Data revealed significant differences of the subjective sensations between the CS+ and CS-, but no differences in the amplitudes and latencies of the P50, N100, P200, and P300 AEP components. No changes in the topographical organization of the CS+ and CS- were found. A significant differential negativity in the brain sites responsible for processing the UCS was obtained, which is attributed to the anticipation of the UCS after CS+ presentation.
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PMID:Classical conditioning of pain responses. 782 88

The pain components of somatosensory evoked potentials (SEPs) of induced by median nerve stimulation were studied with the way of blocking bloodstream of arm in 12 normal adults. The SEPs following the painful stimuli (0.1 msec. square wave pulse) of the right wrist were recorded from the left parietal (C3') and frontal (F3) scalp with earlobe reference electrode. The pressure of 40 mmHg above the arterial pressure was given to the right upper arm by sphygmomanometer. The result showed that the P200-N300 components (latency 234 +/- 13 msec. and 308 +/- 23 msec.) of the SEPs persisted and the others disappeared when tactile sensation disappeared but pain existed. The morphology of P200-N300 from F3 was same to that from C3'. It suggested the P200-N300 were the pain potentials of median nerve SEPs.
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PMID:[The pain components of somatosensory evoked potentials induced by median nerve stimulation P200-N300]. 808 75

Research on the effects of the self-regulation of event-related potentials (ERP) has failed to investigate the possible interactions and contributions of slower cortical events such as contingent negative variations (CNV) and slower DC level changes. The present study attempted to investigate such interactions by independently conditioning the ERP 200 ms poststimulus (P200) and the CNV while recording both potentials simultaneously; DC level measures were also recorded. 30 subjects attempted to increase (uptraining) or decrease (downtraining) either P200 or CNV in response to sub-painful somatosensory stimulation in a biofeedback paradigm. Following the training sessions, P200 downtrainees reported a significant decrease in their detection thresholds for the somatosensory stimuli (i.e., increased sensitivity). These results agree with some prior findings that decreased ERP amplitude in individuals is indicative of greater sensitivity in subjective pain reports. Although uptraining resulted in larger P200 amplitudes than downtraining, the difference in amplitudes between groups was not significant. CNV uptrainees achieved a higher level of pain tolerance following training. The increased CNV negativity may be associated with increased specific attentional processes that facilitate the subjects' control of, or response to, pain. CNV trainers showed a significant interaction of training over blocks of trials. Generally, there was a significant inverse correlation of P200 and CNV; as CNV amplitude became more negative, the P200 amplitude increased. DC negativity level increased over blocks for all conditions. Results indicate a complex relationship between P200, CNV and pain sensitivity. Both P200 and CNV processes are involved in pain perception, but in apparently different ways, i.e., P200 with sensitivity and CNV with tolerance.
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PMID:The self-regulation of slow potential shifts and evoked potentials: interrelationships in response to somatosensory stimulation. 820 6

This study attempted to replicate and extend earlier work that reported that the amplitude of the P200 peak of the human somatosensory evoked potential (SEP) can be increased and decreased when reward is made contingent upon change and that these changes are accompanied by alterations in pain sensitivity. Twenty-one subjects were able to make the amplitude of the P200 peak evoked by sural nerve stimulation larger during increased training (up-training) than during decreased training (down-training). There were no differences in the sural nerve compound action potential between up-training and down-training. This finding demonstrates that the change in P200 amplitude was not due to a change in stimulus efficacy, but rather to a change within the central nervous system. Subjective pain ratings and a nociceptive spinal reflex were the same in up-training as in down-training. Thus, conditioned changes in P200 amplitude do not alter pain sensitivity.
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PMID:Effects of operantly conditioning the amplitude of the P200 peak of the SEP on pain sensitivity and the spinal nociceptive withdrawal reflex in humans. 893 94

In this study, we examined cognitive function during experimental pain induced by an ischemic upper-arm tourniquet. During pain and control conditions, individuals performed a memory search task and an oddball task. Reaction time, errors, and event-related potentials in response to task stimuli were evaluated. Pain reduced accuracy and changed the response-type dependency of errors and the reaction time within the memory search task: false rejections but not false acceptances increased, and rejections were faster than acceptances during pain, whereas the opposite occurred during control conditions. The memory probes elicited an N275 that increased and a P300 that decreased in amplitude during pain. Pain also reduced amplitudes of P200 and P300 from the oddball task. N275 enhancement was greater in nonaffected than affected individuals, suggesting its association with focused attention that inhibited disruption by pain. P300 attenuation is interpreted as an indication that cognitive involvement in pain diminishes the attention resources allocated to a concurrent cognitive task.
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PMID:Event-related potential correlates of interference between cognitive performance and tonic experimental pain. 926 Apr 96

Fifteen adults with chronic low back pain (M = 4 years), age 18 to 43 years (M = 29 years), participated. All but one were moderately to highly hypnotizable (M = 7.87; modified 11-point Stanford Hypnotic Susceptibility Scale, Form C [Weitzenhoffer & Hilgard, 1962]), and significantly reduced pain perception following hypnotic analgesia instructions during cold-pressor pain training. In Part 1, somatosensory event-related potential correlates of noxious electrical stimulation were evaluated during attend and hypnotic analgesia (HA) conditions at anterior frontal (Fp1, Fp2), midfrontal (F3, F4), central (C3, C4), and parietal (P3, P4) regions. During HA, hypothesized inhibitory processing was evidenced by enhanced N140 in the anterior frontal region and by a prestimulus positive-ongoing contingent cortical potential at Fp1 only. During HA, decreased spatiotemporal perception was evidenced by reduced amplitudes of P200 (bilateral midfrontal and central, and left parietal) and P300 (right midfrontal and central). HA led to highly significant mean reductions in perceived sensory pain and distress. HA is an active process that requires inhibitory effort, dissociated from conscious awareness, where the anterior frontal cortex participates in a topographically specific inhibitory feedback circuit that cooperates in the allocation of thalamocortical activities. In Part 2, the authors document the development of self-efficacy through the successful transfer by participants of newly learned skills of experimental pain reduction to reduction of their own chronic pain. Over three experimental sessions, participants reported chronic pain reduction, increased psychological well-being, and increased sleep quality. The development of "neurosignatures of pain" can influence subsequent pain experiences (Coderre, Katz, Vaccarino, & Melzack, 1993; Melzack, 1993) and may be expanded in size and easily reactivated (Flor & Birbaumer, 1994; Melzack, 1991, 1993). Therefore, hypnosis and other psychological interventions need to be introduced early as adjuncts in medical treatments for onset pain before the development of chronic pain.
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PMID:Hypnotic analgesia: 1. Somatosensory event-related potential changes to noxious stimuli and 2. Transfer learning to reduce chronic low back pain. 943 5


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