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

In order to understand the neuronal mechanisms involved in acute and chronic pain, we studied the thalamic and cortical control action, which allows the suppression of the neuronal responses to noxious stimulation. As an experimental pain model we used carrageenin injected in the paw of male Wistar rats. The tonic facilitatory cortical control on centralis lateralis thalamic nuclei (CL) activity is described at different times after carrageenin-produced inflammation. Simultaneous extracellular unit recordings were carried out at CL and medial prefrontal cortex (PCx) cells in anesthetized male Wistar rats. The PCx control was tested by blocking in a transient and reversible manner, using the cortical spreading depression (CSD). Carrageenin injection (1%; 0.2 ml) into the plantar surface of the right hind paw, and the influence of Lidocaine (2%; 0.2 ml) applied in the inflamed paw, was tested on unit activity in PCx and CL cells. Thalamic cells recorded in acute and subacute stages (24-72 h after carrageenin administration) were activated by tactile, light pressure and joint movement stimulation yielded before the injection. After carrageenin, the thalamic cells displayed spontaneous high frequency burst discharges, also presenting a progressive and significant increase (p < 0.001, ANOVA test) of their spontaneous firing rate when compared with control cell activity. Lidocaine reduced the enhanced activity induced by carrageenin in thalamic neurones (p < 0.001, Student t test). In PCx neurones were also recorded in acute and subacute stages. Cortical cells from acute and subacute group were activated by nociceptive and non-nociceptive stimulation. In acute stage, cortical cells increased their firing rate after carrageenin and we could not observe modifications upon their firing rate due to Lidocaine. The CSD blocked all cortical activity in acute and subacute stages. During the CSDs, overall thalamic activity was suppressed in neurones from acute (91%) and subacute (87%) stages. The blockage was observed when the propagated wave produced by CSD arrived into the medial prefrontal cortex. The CSD also suppressed the PCx and the CL noxious responses evoked by pressure in the receptive field. This study shows the tonic facilitatory control of the PCx upon intralaminar thalamic noxious responses, during acute and subacute stages of carrageenin produced-inflammation. In the literature, it has been proposed that the CL thalamic nuclei and the prefrontal cortex are involved in processing the affective component of pain. It may be possible to suppress the thalamic activity during chronic pain, using the transient and reversible blockage of CSD, giving rise to a reduction in the affective reactions to pain. This could also be a therapeutic alternative in chronic pain treatment.
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PMID:Cortical facilitatory action on centralis lateralis thalamic activity during the development of carrageenin-produced inflammation. 885 81

Ten adult patients hospitalized as a result of major burn injury participated in a study that used a single-subject, repeated reversal design in which subject-reported pain during patient-performed washing was compared with subject-reported pain during nurse-performed washing. Analysis, by repeated-measures ANOVA, of verbal numeric pain scores obtained at regular intervals intraprocedurally, indicated that each of the 10 subjects experienced significantly less pain under the condition of patient-performed washing compared with the condition of nurse-performed washing (p < 0.001 through p < 0.05). The quality of washing did not differ significantly (p < 0.05) between conditions, nor did the amount of opioid medication administered (p < 0.05). Results support the active participation of patients with burn injuries in their dressing changes.
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PMID:Procedural burn pain intensity under conditions of varying physical control by the patient. 888 72

The literature regarding the effect of exercise on pain is equivocal. The purpose of this investigation was to quantify the influence of an acute bout of exercise on pain threshold (PT) and pain ratings (PR). A secondary purpose was to measure heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and state anxiety (SA) responses. Pressure (3000-g force) was applied to the middle digit of the right forefinger for 2 min with the Forgione-Barber pain stimulator before and following (5 min of cycling at 75% VO2max. Quiet rest consisted of sitting quietly for 30 min in a sound-dampened chamber. Order was counterbalanced, randomly assigned, and performed on different days. Data was analyzed with a repeated measures ANOVA for multifactor experiments. PT was significantly higher (P < 0.05) and PR were significantly lower (P < 0.05) in the exercise condition 5 min post-exercise in comparison with quiet rest. Changes in pain perception were accompanied by lower SBP (P < 0.03) and higher HR (P < 0.0001). in the exercise condition. It is concluded that an acute bout of exercise is associated with changes in pain perception.
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PMID:Perception of pain following aerobic exercise. 893 93

Symptoms and signs of temporomandibular disorders were assessed in children enrolled in a randomized controlled trial of early treatment for Class II malocclusion. Children (mean age of 9.8 years) were assigned to a treatment protocol (bionator, n = 60; observation, n = 60; headgear/bite plane, n = 71) using randomized block stratification. Temporomandibular joint (TMJ) sounds, joint capsule pain to palpation, and muscle pain to palpation were scored as binary responses (present/absent in a subject). Determinations were made by blinded, calibrated examiners initially (DC1) and after a Class I molar correction was achieved or 2 years had elapsed (DC3). Univariate relationships among explanatory factors (group assignment, gender, age, time interval between DC1 and DC3, Class II severity, mandibular plane angle, preparatory treatment, whether Class I molar relation was achieved) and binary responses were explored using Chi square tables and ANOVA methods. Logistic regression modeled the relationship between binary responses and the explanatory variables. At DC1, the 3 groups were equivalent in the explanatory variables (P > .05). Subjects with a TMJ sound, joint pain, and/or muscle pain at follow-up were more likely those who had the sign at baseline (P < .01). Early treatment with bionators and headgear/bite planes did not place healthy children without these signs at risk for developing these signs. Only increasing age (for the development of sounds, P < .04) and failure to achieve a Class I molar relation (for development of muscle pain, P < .04) placed sign-free children at greater risk. Subjects with TMJ pain at baseline were 7 times more likely to have pain at follow-up if they had been treated with a headgear/bite plane or observed than if they had been treated with a bionator (P = .007). We conclude that an immediate benefit or risk for children receiving early Class II treatment with bionators and headgear/bite planes with respect to temporomandibular joint function does not exist with the prospect that Class II children with TMJ capsule pain may benefit from bionator therapy.
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PMID:Temporomandibular disorders after early Class II treatment with bionators and headgears: results from a randomized controlled trial. 900 12

This study is a randomized, blinded trial that compares the effectiveness of a new topical anesthetic preparation of 2% mepivacaine and 1:100,000 norepinephrine (Mepivanor); a topical solution of 1% tetracaine, 1:4,000 adrenaline, and 4% cocaine (TAC); and 1% lidocaine infiltration during laceration repair in children. The study was conducted in the emergency department of a large academic children's hospital. Study participants were children 2 years of age or older with a laceration on the face or scalp, 5 cm or less in length, that required suturing. Patients were randomly assigned to receive Mepivanor topical solution, TAC topical solution, or lidocaine infiltration anesthesia prior to laceration repair. Seventy-one patients were enrolled in the study during a 2-month period. Outcome measures assessed pain perceptions using a Visual Analogue Scale (VAS) and a seven-point Likert scale. There was statistical power to detect differences of 1.2 to 1.7 units for the VAS outcome measures using alpha = 0.05 and beta = 0.20. There were no statistically significant (P > 0.05) differences between TAC and 1% lidocaine infiltration in providing effective anesthesia. Mepivanor was generally less effective in providing adequate anesthesia during laceration repair than TAC and lidocaine infiltration, with Tukey's post hoc test for ANOVA demonstrating statistically significant (P < 0.05) differences between Mepivanor and these agents for research assistant and suture technician VAS scores. Wound blanching was judged to be less with Mepivanor than with TAC, although this difference was not statistically significant. There were no adverse reactions, wound infections, or healing difficulties for any of the patients who received TAC or Mepivanor. It was concluded that non-cocaine-containing Mepivanor was generally less effective than TAC and lidocaine infiltration in providing adequate local anesthesia during laceration repair. TAC containing only 120 mg of cocaine (3 mL of 4% cocaine) was as effective as 1% lidocaine infiltration in providing local anesthesia during laceration repair. This will allow the amount of cocaine in TAC to be reduced, thereby decreasing costs and the likelihood of adverse reactions.
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PMID:Comparison of topical anesthetics with lidocaine infiltration during laceration repair in children. 900 43

Sixty-eight patients (seven men, 61 women) treated for disk displacement without reduction with extraoral mandibular manipulation followed by splint insertion, physical and drug treatment as needed, were re-examined at the end of treatment and after a subsequent period, ranging from 18 to 147 months. Two parameters were considered: 1. degree of spontaneous mandibular opening; and 2. presence of pain (score 1-4). Mean opening was 28.78 mm before treatment, 42.85 mm after treatment and 43.5 mm at long-term (P < .001 after paired T-test and one-way ANOVA). Mean pain level dropped from 2.91 before treatment to 1.22 after treatment and 1.38 at long-term (P < .001 after Friedman non-parametric test). It was concluded, that in the majority of cases, disk displacement without reduction can successfully be treated by conservative means.
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PMID:Long-term results in patients with disk displacement without reduction treated conservatively. 911 Jun 24

The magnitude of tolerance and dependence is defined in part by agonist concentration and duration of receptor exposure. Therefore, in the face of continued exposure to an opioid agonist, periodic reduction in opiate receptor occupancy should reduce tolerance. Alternately, we have shown that reversal of opiate agonist action yields increased glutamate release and NMDA-antagonist studies indicated that this release may lead to an exacerbation of tolerance. To address this issue, we observed the effect of transient daily antagonism by naloxone of otherwise continuous opioid receptor exposure on morphine tolerance development. Rats with intrathecal (i.t.) catheters and osmotic minipumps were assigned to one of the following 7-day infusion/treatment groups: group A: i.t. morphine (20 nmol/h) with daily subcutaneous (s.c.) injection of naloxone 0.6 mg/kg, group B: i.t. morphine (20 nmol/h) with daily s.c. saline, group C: i.t. saline (1 microl/h) with daily s.c. injection of naloxone 0.6 mg/kg, or, group D: i.t. saline (1 microl/h) with daily s.c. saline. Hot plate response latency was measured daily before and after the s.c. injection. The infusion was discontinued on day 7 and on day 8 the response of the rat to a probe dose of i.t. morphine (60 nmol) given as a bolus was observed. Elevated hot plate latencies were observed for groups A and B on day 1 of infusion and this declined over the following 3-4-day interval. Group B approached baseline, but by day 5 group A showed a mild hyperalgesia prior to each naloxone injection. Groups C and D showed no change in baseline latency. On day 8, 24 h after termination of morphine infusion, the magnitude of the analgesic response to the probe i.t. morphine was: group D = group C > group B > group A (P < 0.05, 1-way ANOVA). Thus, in contrast to the expectation that tolerance would be reduced by periodic blockade of opiate receptor occupancy, rats that had daily transient receptor antagonism showed a greater tolerance than rats with simple continuous receptor occupancy. These results are, however, consistent with work showing that (i) naloxone will evoke spinal glutamate release in spinal morphine tolerant rats and (ii) spinal NMDA receptor antagonism ameliorates loss of opiate effect in this spinal infusion model.
Pain 1997 Apr
PMID:Effect of transient naloxone antagonism on tolerance development in rats receiving continuous spinal morphine infusion. 915 Feb 85

Neuroma formation at the proximal end of a divided nerve is a common problem in peripheral nerve surgery. Forty-eight nerve endings in 23 patients with traumatic or post-elective surgery amputation stumps were capped with either an epineural ligature, epineural flaps or an epineural graft. Each technique was used on 16 nerve endings. After at least 6 months follow-up, pain at the nerve endings was assessed by tapping the treatment sites and asking the patients to score their pain on a visual analogue scale (VAS) from 0 to 10. The mean VAS scores were 5.18 for epineural ligatures, 4.25 for epineural flaps and 2.06 for epineural grafts. Epineural grafts were significantly more effective in preventing neuroma pain (ANOVA: F = 11.4, P < 0.05).
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PMID:Prevention of painful neuromas by epineural ligatures, flaps and grafts. 917 5

Subcutaneous (s.c.) injection of formalin induces a rapid and prolonged hyperalgesia across widespread areas of the body. This hyperalgesic state involves a brain-to-spinal cord pathway, likely arising from the nucleus raphe magnus. The present study examined whether subsequent activation of spinal cord glia may be critical for the hyperalgesic state to be observed in rats. Glia were considered candidates as they can, upon activation, release a variety of substances known to be critical for the mediation of subcutaneous formalin-induced hyperalgesia including glutamate, aspartate, nitric oxide, arachidonic acid and cyclooxygenase products such as prostaglandins. This series of experiments demonstrate that formalin-induced hyperalgesia in rats can be blocked by intrathecal administration of agents that: (a) disrupt glial function (using either 1 nmol fluorocitrate which is a glial metabolic inhibitor, or 9 microg CNI-1493 which disrupts synthesis of nitric oxide and cytokines in monocyte-derived cells; ANOVA revealed reliable group effects for each drug with P < 0.0005); or (b) disrupt the action of glial products (using 10, 50, or 100 microg of a human recombinant interleukin-1 receptor antagonist or 10 microl antibody directed against nerve growth factor; ANOVA revealed reliable group effects for each drug with P < 0.001). Disruption appeared to be selective, as blockade of only select glial products was effective. That is, up to 120 microg of a functional antagonist of tumor necrosis factor-alpha (TNF binding protein) and 5 microl of an antibody against complement-3 produced no statistically reliable reduction in formalin-induced hyperalgesia. Taken together, the present series of experiments suggest an important role for spinal glial cells in the cascade of events that are initiated by descending signals following s.c. administration of formalin.
Pain 1997 Jul
PMID:Evidence for the involvement of spinal cord glia in subcutaneous formalin induced hyperalgesia in the rat. 923 65

The objectives were: (i) to present a method for assessing muscle pain during exercise, (ii) to provide reliability and validity data in support of the measurement tool, (iii) to test whether leg muscle pain threshold during exercise was related to a commonly used measure of pain threshold pain during test, (iv) to examine the relationship between pain and exertion ratings, (v) to test whether leg muscle pain is related to performance, and (vi) to test whether a large dose of aspirin would delay leg muscle pain threshold and/or reduce pain ratings during exercise. In study 1, seven females and seven males completed three 1-min cycling bouts at three different randomly ordered power outputs. Pain was assessed using a 10-point pain scale. High intraclass correlations (R from 0.88 to 0.98) indicated that pain intensity could be rated reliably using the scale. In study 2, 11 college-aged males (age 21.3 +/- 1.3 yr) performed a ramped (24 W.min-1) maximal cycle ergometry test. A button was depressed when leg muscle pain threshold was reached. Pain threshold occurred near 50% of maximal capacity: 50.3 (+/- 12.9% Wmax), 48.6 (+/- 14.8% VO2max), and 55.8 (+/- 12.9% RPEmax). Pain intensity ratings obtained following pain threshold were positively accelerating function of the relative exercise intensity. Volitional exhaustion was associated with pain ratings of 8.2 (+/- 2.5), a value most closely associated with the verbal anchor "very strong pain." In study 3, participants completed the same maximal exercise test as in study 2 as well as leg cycling at 60 rpm for 8 s at four randomly ordered power outputs (100, 150, 200, and 250 W) on a separate day. Pain and RPE ratings were significantly lower during the 8-s bouts compared to those obtained at the same power outputs during the maximal cycle test. The results suggest that noxious metabolites of muscle contraction play a role in leg muscle pain during exercise. In study 4, moderately active male subjects (N = 19) completed two ramped maximal cycle ergometry tests. Subjects drank a water and Kool-Aid mixture, that either was or was not (placebo) combined with a 20 mg.kg-1 dose of powdered aspirin 60 min before exercise. Paired t-tests revealed no differences between conditions for the measures of exercise intensity at pain threshold [aspirin vs placebo mean (+/- SD)]: power output: 150 (+/- 60.3 W) versus 153.5 (+/- 64.8 W); VO2: 21.3 (+/- 8.6 mL.kg-1.min-1) versus 22.1 (+/- 10.0 mL.kg-1.min-1); and RPE: 10.9 (+/- 3.1) versus 11.4 (+/- 2.9). Repeated measures ANOVA revealed no significant condition main effect or condition by trial interaction for pain responses during recovery or during exercise at 60, 70, 80, 90, and 100% of each condition's peak power output. It is concluded that the perception of leg muscle pain intensity during cycle ergometry: (i) is reliably and validly measured using the developed 10-point pain scale, (ii) covaries as a function of objective exercise stimuli such as power output, (iii) is distinct from RPE, (iv) is unrelated to performance of the type employed here, and (v) is not altered by the ingestion of 20 mg.kg-1 acetylsalicylic acid 1 h prior to the exercise bout.
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PMID:Naturally occurring muscle pain during exercise: assessment and experimental evidence. 926 56


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