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

A patient with chronic pain and DSM-III unipolar and cyclothymic disorders was treated with L-tryptophan, 3000 mg before bed for 3 nights, and showed no response. She then began to take L-tryptophan, 1000 mg every 4 hours, with a high carbohydrate, low protein meal and immediately showed a clear improvement in exercise tolerance (reduced pain) and alleviation of affective symptoms. The importance of pharmacokinetic factors in the clinical use of L-tryptophan is emphasized.
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PMID:Pharmacokinetic factors in the clinical use of tryptophan. 651 6

Fifty consecutive patients requiring nonsurgical endodontic therapy were the subjects of this pain-control study. Twenty-five subjects received 3 gm of tryptophan in divided 0.5-gm doses over a 24-hour period, beginning before the start of treatment. The other twenty-five subjects received an identically appearing placebo on the same dosage schedule. Pain intensity was evaluated by the subjects on a scale of 0 to 10 (0 = no pain, 10 = severe pain) (1) prior to the start of treatment, (2) after 24 hours, and (3) 1 week later. Results showed that the most meaningful difference was found at 24 hours, when the tryptophan group was significantly better than the placebo group (F = 7.46, df = 1.96, p less than 0.01).
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PMID:The effect of tryptophan on postoperative endodontic pain. 659 75

The effects of a nociceptive peripheral stimulus and/or morphine upon endogenous tryptophan levels (TRP), specific activity of tryptophan (S.A. of TRP) and serotonin (5-HT) synthesis in the dorsal and ventral spinal cord, the brainstem and the forebrain were investigated in anaesthetized rats. Whereas endogenous TRP and S.A. of TRP were not found to be affected by any of the manipulations described below, 5-HT synthesis was markedly altered. The application of a prolonged and intense nociceptive electrical stimulus to the tail induced a rise in 5-HT synthesis which was dependent on the part of the CNS considered, with the dorsal cord being the most sensitive (25%), the ventral cord and the brainstem being effected to a lesser extent (14% and 16% respectively), and the forebrain not being affected significantly. By contrast, the application of a prolonged and innocuous electrical stimulus on the tail was not followed by any detectable changes in 5-HT synthesis. Morphine administration (1 mg/kg; i.v.) did not significantly alter 5-HT synthesis in the four CNS regions considered. Nevertheless, the same morphine dose did induce a highly significant (P less than 0.005) reduction in the increase in 5-HT synthesis induced by the nociceptive stimulus, both in the dorsal cord and in the brainstem. Such an effect was not seen in the ventral cord. The specificity of these morphine effects was demonstrated by their naloxone reversibility; on the other hand, naloxone alone failed to modify the stimulus-induced increase in 5-HT synthesis seen in the dorsal cord and the brainstem. The results, particularly those concerning the dorsal cord, are discussed with reference to pain mechanisms and morphine analgesia. They suggest that peripheral nociceptive messages induce an increased activity in some bulbo-spinal 5-HT pathways and that a low dose of morphine can counteract such an effect. It is proposed that exogenous opiates exert a complex regulation of bulbo-spinal 5-HT pathways. Functional significances of these processes are discussed.
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PMID:Increase in 5-HT synthesis in the dorsal part of the spinal cord, induced by a nociceptive stimulus: blockade by morphine. 672 43

Morphine analgesia measured by the tail withdrawal test was examined in rats that were either restrained or left free during testing. It was found that restraint potentiated morphine analgesia and decreased the latency of the peak analgesic effect. Methysergide, a serotonin antagonist, and valine, which prevents the increase in brain tryptophan induced by restraint, blocked the effect of restraint on morphine analgesia. Valine did not alter analgesia in unrestrained rats. An increase in brain tryptophan uptake induced by stress is suggested as a possible mechanism by which stress can interact with pain modulation systems.
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PMID:Evidence that stress augments morphine analgesia by increasing brain tryptophan. 672

We examined the behavioral effects of the dietary constituents tryptophan and tyrosine on human mood, sensorimotor performance and pain sensitivity. Tryptophan and tyrosine are neurotransmitter precursors present in varying amount in protein-containing foods. Tryptophan (50 mg/kg) increased subjective drowsiness and fatigue but unlike many hypnotics did not impair sensorimotor performance. Tryptophan also decreased human pain sensitivity in a manner that was more specific than certain analgesic drugs.
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PMID:Mood, performance, and pain sensitivity: changes induced by food constituents. 676 30

This study investigated the effects of daily administration of three grams of tryptophan in conjunction with a high carbohydrate, low fat, low protein diet on chronic maxillofacial pain, experimental pain thresholds, and anxiety and depression. In a double-blind study, 30 chronic pain patients were randomly assigned to a tryptophan or placebo group. At the initial appointment and 4 weeks later, the patients' subjective ratings of their pain were recorded, electrical tooth pulp stimulation was used to measure pain thresholds, and psychological tests of depression and anxiety were administered. Over the 4 weeks of the study, there was a greater reduction in reported clinical pain and a greater increase in pain tolerance threshold in the tryptophan group than in the placebo group. The group did not differ in anxiety and depression--for all subjects there was lowered depression and anxiety over the 4 weeks of study.
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PMID:The effects of dietary tryptophan on chronic maxillofacial pain and experimental pain tolerance. 676 35

5,7-Dihydroxytryptamine (5,7-DHT), median raphe nucleus (MRN)-lesioned and sham-lesioned rats were submitted to one-trial passive avoidance conditioning followed by electroconvulsive shock (ECS) or sham-ECS. On test session (24 h later) MRN-lesioned rats presented a longer conditioned response and, chiefly, a remarkable reduction of ECS-induced retrograde amnesia in comparison to sham-lesioned animals. This effect appeared unrelated to major changes in spontaneous behavior: on training session MRN-lesioned rats exhibited a faster stepping-down from the platform; their exploratory activity into a novel cage was characterized by a slightly higher initial response; moreover MRN lesion did not significantly effect pain threshold. A reduced brain 5-HT functional activity following MRN lesion was suggested by the study of the hyperactivity syndrome induced by tranylcypromine plus L-tryptophan. Lastly, MRN-lesioned rats showed a significantly lower brain 5-HT steady level without differing from the sham-lesioned ones with respect to turnover rate. The reduction of ECS-induced retrograde amnesia observed in 5,7-DHT, MRN-lesioned rats was considered as due to a lower synaptic availability of 5-HT at the time of ECS administration.
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PMID:Reduction of ECS-induced retrograde amnesia of passive avoidance conditioning after 5,7-dihydroxytryptamine median raphe nucleus lesion in the rat. 696 65

Pain perception and tolerance thresholds of 30 normal subjects were determined by electrical stimulation of dental pulps before and after dietary manipulation which included either tryptophan supplementation or placebo. Perception threshold levels were similar in tryptophan and placebo subjects; however, pain tolerance levels were significantly higher in the group receiving tryptophan. Side effects such as nausea, skin itching, weight loss and mood elevation were more common in the tryptophan group than in the placebo group.
Pain 1982 Aug
PMID:Alteration of human pain thresholds by nutritional manipulation and L-tryptophan supplementation. 713 33

The effects of dietary excesses of tryptophan, histidine, tyrosine or choline and of a tryptophan-free diet were examined on shock-induced fighting, muricide and jump-flinch thresholds. Following the tryptophan-free diet, shock-induced fighting and pain sensitivity were specifically increased. The increased incidence of muricide was not specific to the lack of tryptophan in the diet. Groups of rats which were pair fed chow or had 0.15% L-tryptophan added to the tryptophan-free diet increased muricide as well. Brain 5-HT levels were 41% depleted following the tryptophan-free diet and reduced 13% with the 0.15% tryptophan supplement. In addition body weights were reduced in the three groups compared to control. None of the excess diets affected shock-induced fighting, muricide and jump-flinch thresholds. Body weights were decreased in the excess tryptophan, histidine, tyrosine and choline groups. These data indicate that the expression of different forms of aggression appears to be influenced by a tryptophan deficiency in the diet, but not by excesses of tryptophan, tyrosine, histidine and choline.
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PMID:Effects of dietary supplements and a tryptophan-free diet on aggressive behavior in rats. 718 91

Five patients on chronic opiate medication to treat low-back and leg pain were determined to have developed opiate tolerance on the basis of their failure to obtain significant relief (rated on a subjective pain scale and by the degree of straight leg-raising they were able to endure) after receiving 30 mg of morphine administered i.v. in divided doses over 35 min. After these patients' diets had been supplemented with 4 g/day of L-tryptophan for 2-9 weeks, they achieved significant relief from pain when the opiate tolerance test was re-administered, and were able to lead more active lives while reducing their daily opiate intake. chronic opiate administration probably reduces the serotonin turnover rate in the central nervous system; it may be that this is reversed by loading with the serotonin precursor, L-tryptophan.
Pain 1980 Oct
PMID:Tryptophan loading may reverse tolerance to opiate analgesics in humans: a preliminary report. 745 82


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