Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatosensory (SEP), auditory evoked potentials (AEP) and power spectral density of ongoing EEG (PSD) were investigated under different drug conditions: the opioid pentazocine (30 mg), the centrally acting non-narcotic analgesic flupirtine (80 mg) and placebo were administered i.v. in a double-blind cross-over study (intersession interval 7 days) with 20 healthy male subjects. Intracutaneous electrical stimuli were applied to the finger tip with randomized intensities of two- and threefold individual pain threshold. One stimulus block consisted of 80 trials. Mean values of two stimulus blocks per session were analyzed: one block before and one block 30 min after treatment. Pentazocine significantly reduced the peak-to peak amplitude of the late SEP components (N150-P240) from pretreatment to posttreatment blocks, and flupirtine diminished this amplitude to nearly the same degree. With placebo no substantial reduction was found. In contrast to these drug-induced changes in SEP, the AEP components showed no significant alterations after any treatment. The PSD under pentazocine showed a reduction of total power. This effect was mainly due to a reduced power in the alpha band. The PSD under flupirtine showed slight increases in power of theta, alpha and beta activity. Again, under placebo no changes from pretreatment to posttreatment conditions occurred. The difference in EEG change might suggest different sites of action of the two analgesics.
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PMID:Pentazocine and flupirtine effects on spontaneous and evoked EEG activity. 358 74

The potentials (EPs) evoked by cutaneous electric shock of increasing intensity and the corresponding sensitivity thresholds were studied in 25 healthy volunteers: analgesic electrical stimulation (AES) was performed on only 10 of these. The stimuli (0.5 msec; 0-140 V) applied in a random way with a needle electrode implanted in the horny layer of the tip of the middle finger can produce 4 sensations: initial awareness, pressure sensation, diffusion and pain. The EP recorded on the somatosensory areas had the typical somatosensory (SEP) morphology only at the pressure stage. At the pain thresholds, the response was a well-demarcated 'nociceptive' EP (NEP), with main components at P100, N140, P240. After 45 min of AES, the increase of the sensitivity thresholds was peculiarly pronounced for that of pain, homolaterally (80%) and contralaterally (45%) to the AES. With respect to the EPs, the NEP and especially its late waves showed a noteworthy reduction in amplitude, more significant on the homolateral side (66%) than on the contralateral one (50%), whilst the SEP was only slight modified. The evolution of the thresholds and of the EPs was followed for 45 min after cessation of AES and revealed a significant residual effect of comparable values for the two parameters.
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PMID:[Changes in cortical evoked potentials in relation to cutaneous sensory thresholds. Application to a study of analgesic electrostimulation]. 387 79

In a group a patients with a pain syndrome in spinal cord injury electric stimulation of n. medianus causes the appearance of a component of a somatosensory induced potential (IP) which is a high-amplitude superficial-positive oscillation with a latent peak period of 200-280 mc. A similar oscillation is revealed in a group of healthy individuals in response to nociceptive stimulation of the skin on the forearm. The amplitude of this potential reduced markedly in effective antipain stimulation through electrodes implanted into the posterior columns of the spinal cord. In the absence of an antipain effect the oscillation described persisted at the time of the patient's discharge from the clinic. The existence of a connection between the described potential (P240) with the pain syndrome and the perception of pain stimulation is suggested. On the basis of the data obtained the possibility of objectifying the intensity of the pain sensations by somatosensory IP recording is contemplated.
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PMID:[Attempt at objective evaluation of pain and analgesia during stimulation of the posterior columns in patients with spinal cord lesions]. 633 27

We investigated effects of sleep on pain-related somatosensory evoked potentials (SEP) following painful electrical stimulation of the left index finger. The biggest advantage of this method is that signals ascending through both A-beta fibers relating to touch and A-delta fibers relating to pain can be recorded simultaneously. While the subject was awake, non-painful stimulation evoked early- and middle latency components, N20, P30 and N60, at the C4 electrode, and painful stimulation evoked not only early- and middle latency components at the C4 but also later pain-specific components, N130 and P240, at the Cz electrode. During sleep, N20 and P30 did not show a significant change in amplitude, N60 showed a slight but significant amplitude reduction, and N130 and P240 significantly decreased in amplitude or disappeared, as compared with those while awake. Therefore, we speculate on the mechanisms generating each component as follows; (1) N20 and P30 are the primary components generated in SI ascending through A-beta fibers. (2) N60 is the secondary component generated in SI involving cognitive function to some degree. (3) N130-P240 are the pain-specific components ascending through A-delta fibers, and closely related to cognitive function, because they were much affected by consciousness, different from the components ascending through A-beta fibers.
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PMID:Effects of sleep on pain-related somatosensory evoked potentials in humans. 1250 24

Secondary hyperalgesia is believed to be a key feature of "central sensitization" and is characterized by enhanced pain to mechanical nociceptive stimuli. The aim of the present study was to characterize, using EEG, the effects of pinprick stimulation intensity on the magnitude of pinprick-elicited brain potentials [event-related potentials (ERPs)] before and after secondary hyperalgesia induced by intradermal capsaicin in humans. Pinprick-elicited ERPs and pinprick-evoked pain ratings were recorded in 19 healthy volunteers, with mechanical pinprick stimuli of varying intensities (0.25-mm probe applied with a force extending between 16 and 512 mN). The recordings were performed before (T0) and 30 min after (T1) intradermal capsaicin injection. The contralateral noninjected arm served as control. ERPs elicited by stimulation of untreated skin were characterized by 1) an early-latency negative-positive complex peaking between 120 and 250 ms after stimulus onset (N120-P240) and maximal at the vertex and 2) a long-lasting positive wave peaking 400-600 ms after stimulus onset and maximal more posterior (P500), which was correlated to perceived pinprick pain. After capsaicin injection, pinprick stimuli were perceived as more intense in the area of secondary hyperalgesia and this effect was stronger for lower compared with higher stimulus intensities. In addition, there was an enhancement of the P500 elicited by stimuli of intermediate intensity, which was significant for 64 mN. The other components of the ERPs were unaffected by capsaicin. Our results suggest that the increase in P500 magnitude after capsaicin is mediated by facilitated mechanical nociceptive pathways.
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PMID:Characterizing pinprick-evoked brain potentials before and after experimentally induced secondary hyperalgesia. 2633 10