Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three different techniques for producing multiple intercostal nerve blocks using bupivacaine were compared in volunteers. The techniques used were multiple injections at intercostal nerves 7-11, or a single injection employing a needle or a catheter inserted in the 9th intercostal space. The injections were made at the costal angle. The anatomical spread of a mixture of a local anaesthetic and a radio-opaque fluid following the single injection technique at the ninth intercostal space or at the subcostal space was evaluated by computerized x-ray tomography (CT). The distribution of cutaneous analgesia/hypalgesia following all techniques was evaluated by pin prick. No spread of the local anaesthetic to adjacent intercostal spaces or to the paravertebral space could be shown by CT. The distribution of cutaneous analgesia was limited to three segments or less following a single injection. No difference in blood levels of bupivacaine could be found. It is concluded that the single injection technique of producing multiple intercostal nerve blocks is inferior to the multiple injection technique.
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PMID:Multiple intercostal blocks by a single injection? A clinical and radiological investigation. 403 38

Various stresses (i.e. transfer stress, exposition of animals to a new environment, footshock stress, anticipation stress) were found to produce hypalgesia as judged from an increase of the tail - flick latency in rats. Hypalgesia induced by transfer stress was slightly reduced by diazepam (5 mg per kg), but very significantly by chlorpromazine (5 mg per kg). Footshock-stress-induced analgesia lasted less than 15 min. Because naloxone or dexamethasone did not block the footshock-induced analgesia, the participation of the endorphinergic system in this form of stress-induced analgesia is not probable. During the 30 min lasting conditioned reaction to footshock administration (called here anticipation stress), marked analgesia was observed. This anticipation-stress-induced analgesia was blocked by naloxone, dexamethasone and chlorpromazine; no blockade was observed after diazepam. These observations suggest that the endorphinergic system in this form plays a role in stress-induced analgesia. The comparison of the effects of naloxone and/or dexamethasone on the analgesia induced by footshock on the one hand and analgesia induced by anticipation stress on the other thus suggests that different antinociceptive mechanisms are activated by the unconditioned and/or conditioned stimulus.
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PMID:Analgesia induced by painful stimulation and/or anticipation of pain; different mechanisms are operating. 653 79

The effects of epinephrine 1/200,000 as an adjuvant to epidural morphine were investigated in three healthy male volunteers, during 26-h observation sessions. Peak blood concentrations of morphine were 44 +/- 12.9 ng/ml after plain morphine and 13.7 +/- 6.7 ng/ml after epinephrine-morphine. Cutaneous hypalgesia was more intense, faster in onset, and longer in duration after epinephrine-morphine than after plain morphine, and analgesia to ice-water immersion of extremities lasted longer. Adverse side effects of pruritus, nausea, vomiting, and difficulty of micturition were also more intense after epinephrine-morphine, and respiratory sensitivity to CO2 was depressed more severely between 6 and 16 h. The results indicated that epinephrine 1/200,000 reduces vascular absorption of epidural morphine and intensifies all the manifestations of cord and brainstem uptake.
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PMID:Influence of epinephrine as an adjuvant to epidural morphine. 682 60

Ten healthy males between 18 and 33 years received 10 mg morphine sulfate intravenously, or by lumbar epidural injection at two sessions 2-4 weeks apart, in random sequence. The following observations were made at intervals for 22 h. (1) Segmental hypalgesia to ice and pin scratch. (2) Cold pressor response test in hand and foot as an index of analgesia. (3) Time of onset and duration of side effects. (4) Serum concentrations of morphine. Few non-respiratory changes were seen after intravenous morphine. Cold pressor response was unchanged in hand and foot, no segmental hypalgesia or itching occurred, and only one subject complained of nausea. Marked changes occurred after epidural morphine. Cutaneous hypalgesia to ice and pin scratch appeared in the thoracolumbar region all subjects. In six subjects hypalgesia rose to the midthoracic region during the second or third hour and to the trigeminal distribution between the sixth and ninth hour in five subjects. Cold pressor response fell rapidly in the foot during the first 1.5 h after epidural morphine, and a little later cold pressor response also fell in the hand in all subjects, and remained depressed for the duration of the experimental period. Pruritus occurred at three hours in nine of the 10 subjects, nausea at about four hours in six of the subjects, and vomiting at about six hours in five of the subjects. Hypalgesia and side effects were not related to serum concentrations of morphine. These results suggest that lumbar epidural morphine travels cephalad in the cerebrospinal fluid to reach the brain stem and fourth ventricle by the sixth hour.
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PMID:Rostral spread of epidural morphine. 708 27

Trigeminal tractotomy near the level of the obex was carried out in 10 macaque monkeys. Behavioral responses were evaluated by a quantitative paradigm measuring lever-press responses to electrical stimulation of the dental pulp or facial skin, and by assessing facial response to cutaneous pin-scratch before and after the tractotomy. Two pharmacological agents, strychnine and L-dopa, were administered and their effect on behavioral responses to these stimuli was studied. Tractotomy did not produce dental analgesia. Thresholds for escape from cutaneous electrical stimulation of facial skin, however, were elevated, consistent with marked hypalgesia to pin-scratch. The adversive responses to pin-scratch were absent in peripheral portions of the face, but near the midline and inside the oral cavity they were usually decreased or normal. Pharmacological agents caused a reduction in escape thresholds to cutaneous electrical stimulation and a shrinkage or abolition of the zone of analgesia to pin-scratch. The results imply that trigeminal nucleus caudalis, which undergoes deafferentation by tractotomy, may not be essential for processing of nociceptive information from the teeth, oral cavity, and midline facial zones. This findings is contrary to long-held hypotheses concerning facial pain mechanisms. The ability of strychnine and L-dopa to alter nociceptive escape thresholds is consistent with the idea, suggested by Denny-Brown, that facial nociception depends on central summation in the entire spinal trigeminal nucleus from overlapping afferent inputs contained in the trigeminal nerve, other cranial nerves, and the upper cervical nerve roots.
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PMID:Effect of trigeminal tractotomy on behavioral response to dental pulp stimulation in the monkey. 726 33

There is a lack of prospective studies for the long-term results of percutaneous stereotactic radiofrequency rhizotomy (PSR) in the treatment of patients with trigeminal neuralgia. The authors present results in 154 consecutive patients with trigeminal neuralgia treated by PSR and prospectively followed for 15 years. Ninety-nine percent of the patients obtained initial pain relief after one PSR. Dysesthesia occurred in 31 patients (23%): in 7% with mild initial hypalgesia; in 15% with dense hypalgesia; and in 36% with analgesia. Dysesthesia was mild and did not require treatment in most patients. The corneal reflex was absent or depressed in 29 patients, and keratitis developed in three patients. In 19 of 22 patients with trigeminal motor weakness, the paresis resolved within 1 year. Of 33 patients who had pain recurrence, 10 patients had pain that was mild or controlled with medications, and 23 patients required additional surgical treatment. The authors estimated using Kaplan-Meier analysis that the 14-year recurrence rate was 25% in the total group: 60% in patients with mild hypalgesia, 25% in those with dense hypalgesia, and 20% in those with analgesia. Timing of pain recurrence varied according to the degree of sensory loss. All pain recurrences in patients with mild hypalgesia occurred within 4 years after surgery; 10% more of the patients with dense hypalgesia had pain recurrences within the first 10 years compared with patients with analgesia. The median pain-free survival rate was 32 months for patients with mild hypalgesia and more than 15 years for patients with either analgesia or dense hypalgesia. Of the 100 patients followed for 15 years after one or two PSR procedures, 95 patients (95%) rated the procedure excellent (77 patients) or good (18 patients). The authors conclude that PSR is an effective, safe treatment for trigeminal neuralgia. Dense hypalgesia in the painful trigger zone, rather than analgesia, should be the target lesion.
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PMID:A prospective 15-year follow up of 154 consecutive patients with trigeminal neuralgia treated by percutaneous stereotactic radiofrequency thermal rhizotomy. 749 Jun 43

Although the primary treatment of chronic cluster headache is medical, surgical treatment is sometimes used. The authors reviewed the charts of seven patients (ages 36 to 68 years) with chronic cluster headache to identify who responded best to percutaneous stereotactic radiofrequency rhizotomy after medical treatment failed. All patients had immediate pain relief after surgery. At follow-up (median 5 years, range 2 to 20 years), two patients remained pain-free 7 and 20 years later (excellent results); three patients had mild pain recurrence that was well controlled on medications (good results) 6 to 12 months after surgery; and two patients had major pain recurrence 4 days and 2 months after surgery (poor results). Six patients had relief of vasomotor symptoms. One patient had transient diplopia and keratitis without permanent sequelae. Both patients with excellent results had preoperative major pain around the eye; both patients with poor results had major pain around the temple, ear, and cheek; and the three patients with good results had pain equally severe in the eye, temple, and cheek. There was no association between patient age or sex, pain duration, preoperative response to lidocaine blockade, or previous surgery with pain relief. No differences occurred in pain relief between patients with dense hypalgesia and patients with analgesia. The authors conclude that (1) some patients with chronic cluster headache treated by percutaneous stereotactic radiofrequency rhizotomy achieve long-term pain relief, and (2) surgery on the trigeminovascular system alone may not cure the condition in patients with major pain around the temple, ear, and cheek.
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PMID:Long-term results of radiofrequency rhizotomy in the treatment of cluster headache. 777 74

Capsaicin applied topically to human skin produces itching, pricking and burning sensations due to excitation of nociceptors. With repeated application, these positive sensory responses are followed by a prolonged period of hypalgesia that is usually referred to as desensitization, or nociceptor inactivation. Consequently, capsaicin has been recommended as a treatment for a variety of painful syndromes. The precise mechanisms that account for nociceptor desensitization and hypalgesia are unclear. The present study was performed to determine if morphological changes of intracutaneous nerve fibers contribute to desensitization and hypalgesia. Capsaicin (0.075%) was applied topically to the volar forearm four times daily for 3 weeks. At various time intervals tactile, cold, mechanical and heat pain sensations were assessed in the treated and in contralateral untreated areas. Skin blisters and skin biopsies were collected and immunostained for protein gene product (PGP) 9.5 to assess the morphology of cutaneous nerves and to quantify the number of epidermal nerve fibers (ENFs). Capsaicin resulted in reduced sensitivity to all cutaneous stimuli, particularly to noxious heat and mechanical stimuli. This hypalgesia was accompanied by degeneration of epidermal nerve fibers as evidenced by loss of PGP 9.5 immunoreactivity. As early as 3 days following capsaicin application, there was a 74% decrease in the number of nerve fibers in blister specimens. After 3 weeks of capsaicin treatment, the reduction was 79% in blisters and 82% in biopsies. Discontinuation of capsaicin was followed by reinnervation of the epidermis over a 6-week period with a return of all sensations, except cold, to normal levels. We conclude that degeneration of epidermal nerve fibers contributes to the analgesia accredited to capsaicin. Furthermore, our data demonstrate that ENFs contribute to the painful sensations evoked by noxious thermal and mechanical stimuli.
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PMID:Topical capsaicin in humans: parallel loss of epidermal nerve fibers and pain sensation. 1035 1

A series of studies with humans as well as experiments carried out on animals have shown that physical exercise leads to temporary hypoalgesia. Reduced sensitivity to pain is not only demonstrable after long-distance exercise (such as a marathon run) but also during and after intensive physical exercise on a laboratory ergometer. In a double blind study (20 mg naloxone versus placebo) experimental pain thresholds (electrical intracutaneous finger and dental pulp stimulation) and plasma hormone levels (beta-endorphin, cortisol, and catecholamines) were measured in ten healthy athletic men before, during, and after physical exercise on a cycle ergometer. A significant pain threshold elevation during exercise was found for finger (Anova,p<0.004) and dental pulp stimulation (p<0.01). Hypoalgesia remained present after exercise was stopped and the initial pain threshold level was returned to approximately 60 minutes after the exercise. The subjective magnitude estimation of suprathreshold stimuli was significantly reduced (p<0.001) after exercise. Naloxone failed to affect pain thresholds and plasma beta-endorphin did not correlate significantly with pain thresholds. The cause of the exercise-induced hypoalgesia is probably an activation of central pain inhibitory mechanisms by the "stimulus" of physical exercise (stimulation-induced analgesia). Central pain inhibitory systems are probably thereby activated by the stimulation of afferent nerves endings (group III and IV) in the skeletal muscle. The same trigger mechanism also plays a role as a release stimulus for hormones which are secreted in increased measure during physical exercise (catecholamines, pituitary hormones). Plasma beta-endorphin is probably not directly involved in the exercise-induced hypoalgesia but is rather a "marker" for the activating of central analgesia mechanisms.
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PMID:[Physical exercise, endogenous opiates and pain regulation.]. 1841 88

Norepinephrine and serotonin involvement in nociceptive functions is supported by observations of analgesic effects of norepinephrine transporter (NET) and serotonin transporter (SERT) inhibitors such as amitriptyline. However, the relative contribution of NET and SERT to baseline nociception, as well as amitriptyline analgesia, is unclear. Amitriptyline and morphine analgesia in wild-type (WT) mice and littermates with gene knockout (KO) of SERT, NET or both transporters was conducted using the hotplate and tail-flick tests. Hypoalgesia was observed in NET KO mice, and to a lesser extent in SERT KO mice. The magnitude of this hypoalgesia in NET KO mice was so profound that it limited the assessment of drug-induced analgesia. Nonetheless, the necessary exclusion of these subjects because of profound baseline hypoalgesia strongly supports the role of norepinephrine and NET in basal nociceptive behavior while indicating a much smaller role for serotonin and SERT. To further clarify the role of NET and SERT in basal nociceptive sensitivity further experiments were conducted in SERT KO and NET KO mice across a range of temperatures. NET KO mice were again found to have pronounced thermal hypoalgesia compared to WT mice in both the hotplate and tail-flick tests, while only limited effects were observed in SERT KO mice. Furthermore, in the acetic acid writhing test of visceral nociception pronounced hypoalgesia was again found in NET KO mice, but no change in SERT KO mice. As some of these effects may have resulted from developmental consequences of NET KO, the effects of the selective NET blocker nisoxetine and the selective SERT blocker fluoxetine were also examined in WT mice: only nisoxetine produced analgesia in these mice. Collectively these data suggest that NET has a far greater role in determining baseline analgesia, and perhaps other analgesic effects, than SERT in mice.
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PMID:A greater role for the norepinephrine transporter than the serotonin transporter in murine nociception. 2112 46


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