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

Aspects of sleep stage evaluation and analysis of alpha and delta EEG frequencies in sleep were shown to be related to musculo-skeletal pain and mood disturbance in patients with 'fibrositis syndrome'. Patients were treated at bedtime for 3 weeks with either chlorpromazine, 100 mg (8 patients), or L-tryptophan, 5 g (7 patients). Chlorpromazine, but not L-tryptophan, was associated with increased slow wave sleep and amelioration of pain and mood symptoms. Mean percent time/min or mean percent power/min of alpha frequency during NREM and REM sleep corrlated with overnight increase in pain measures, hostility, and decrease in energy. On the other hand, mean percent time/min of delta in NREM sleep was related to overnight decrease in pain and mean percent delta power/min was associated with decreased anxiety and hostility, and increased energy.
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PMID:The relationship of alpha and delta EEG frequencies to pain and mood in 'fibrositis' patients treated with chlorpromazine and L-tryptophan. 615 93

This paper reviews the author's nine years of experience in analgesic brain stimulation. During this time, of 22 patients with pain of peripheral origin who were treated with periaqueductal gray (PAG), stimulation 16 achieved successful control of pain. Of 40 patients who presented with deafferentation pain, 16 were able to control their dysesthesia by brain stimulation of the subcortical somatosensory region alone; follow-up was over a long period. The mechanism of deafferentation pain is poorly understood and the effectiveness of subcortical somatosensory electrical stimulation to relieve such pain is based on empirical observation. The analgesia produced by PAG stimulation appears to be mediated by the release of beta-endorphin from the anterior hypothalamus. The released beta-endorphin binds to the opiate receptors in the PAG and activates the descending pain-inhibitory pathway. However, the repetitive stimulation of this serotonergic system produces tolerance to its analgesic effect, due to a decreased rate of serotonin turnover. Loading of the serotonin precursor by dietary supplementation of the essential amino acid L-tryptophan reverses this tolerance.
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PMID:The current status of analgesic brain stimulation. 616 68

In rats suffering from experimentally induced arthritis produced by Freund's adjuvant, there is a marked decrease in total serum tryptophan levels and a marked increase in plasma-free tryptophan levels at both 15 and 21 days after the administration of the adjuvant. Tryptophan, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid levels are increased in the brain and the spinal cord at 15 days. However, 21 days after administration of the adjuvant these levels returned to normal values in the brain, but remained increased in the spinal cord. These results are in agreement with investigations suggesting the possible involvement of the raphe-spinal system in response to pain stimuli but are contrary to the observation that there is a large decrease in plasma-free tryptophan levels in arthritic human patients. These opposite results still question the hypothesis of a relationship between changes in plasma-free tryptophan levels and the severity of pain.
Pain 1980 Dec
PMID:Total and free serum tryptophan levels and brain 5-hydroxytryptamine metabolism in arthritic rats. 616 24

Using two procedures known to enhance shock-induced defensive fighting (SIF) and mouse-killing--septal lesions and 5,7-DHT lesions--we determined if a 5% tryptophan-loaded diet could reverse the lesion effects. The results indicated that SIF, but not mouse-killing, could be maintained at normal levels following dietary tryptophan loading in both septally lesioned and 5,7-DHT lesioned rats. This behavioral reversal was independent of pain sensitivity, feeding, drinking and body weight levels. Regional brain analysis of monoamines and metabolites indicated that the lesions produced substantial depletions in 5-HT and 5-HIAA with minimal reduction or no change in catecholamines. Dietary tryptophan loading elevated 5-HT and 5-HIAA in unlesioned animals and partially restored 5-HT and 5-HIAA levels in lesioned animals. These patterns of depletion and repletion were confined to the hippocampus following septal lesions and distributed throughout the brain following 5,7-DHT lesions. The results are discussed in terms of a possible hippocampal mediation of the dietary tryptophan reversal in shock-induced defensive fighting following lesioning.
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PMID:Dietary tryptophan reversal of septal lesion and 5,7-DHT lesion elicited shock-induced fighting. 617 74

Chronic implantation of a stimulating electrode in the thalamic relay nucleus (11 cases), in the periaqueductal gray (1 case) and in the internal capsule (2 cases) was performed in fourteen cases which suffered from intractable pain. All these cases could get pain relief at least initial two months. Ventricular fluids were collected before and after stimulation with optimal combination of parameters, and measurements of beta-endorphin were performed by radio-immunoassay. Intrathecal morphine (1mg) injection was performed in eight cases. Cerebrospinal fluids were collected by lumbar tap before and 24 hours after morphine injection. beta-endorphin immunoreactivity was measured by the same method. Pain relief was judged to be excellent if the patient so claimed, and if he discontinued analgesics. Pain relief was thought to be good when it was not completely controllable by stimulation but was sufficiently improved that the patient could do without analgesics. It was thought to be fair when patient could not discontinue analgesics, and poor when patient could not get pain relief. We usually attempt to prevent the stimulation-tolerance by administration of the monoamine precursors , i.e., 1-dopa and 1-tryptophan, on the basis of the experimental observation reported previously. In somatogenic pain patients, the thalamic relay nucleus stimulation was performed in 7 cases (excellent; 3, good; 1, fair; 3) and the periaqueductal gray stimulation in one case (good).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Thalamic relay nucleus stimulation for relief of intractable pain. Clinical results and beta-endorphin immunoreactivity in cerebrospinal fluid]. 633 Jun

Animal and human studies indicate that diet can alter plasma and brain concentrations of neurotransmitter precursors, with possible implications for the synthesis and release of brain neurotransmitters. The best known example is serotonin, whose synthesis is limited by the availability of its precursor, tryptophan, in the brain. Consuming tryptophan or a carbohydrate-rich, protein-poor meal increases brain levels of tryptophan and serotonin. Although a carbohydrate meal itself lacks tryptophan, the meal causes insulin to be secreted. Insulin, in turn, decreases plasma levels of large neutral amino acids that would ordinarily compete with tryptophan for transport across the blood-brain barrier. Resulting brain changes in serotonin provide a plausible mechanism whereby diet could affect behaviour. Research on human subjects suggests that ingesting tryptophan or carbohydrate can reduce subjective alertness and possibly influence some aspects of objective performance. Effects on sleep latency and on pain perception have also been detected. Behavioral effects may come about via the action of tryptophan on brain serotoninergic pathways, although other mechanisms may operate and must still be ruled out before the mechanism is certain.
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PMID:Recent research on the behavioral effects of tryptophan and carbohydrate. 640 41

Recent studies have shown that while the analgesic responses induced by certain stressors appear to be related to morphine analgesia, the analgesic responses to other stressors do not. Para-chlorophenylalanine (PCPA), a potent tryptophan-hydroxylase inhibitor has been shown to decrease both basal pain thresholds and morphine analgesia on the flinch-jump test. To assess further the relationship between morphine and stress-induced analgesia, PCPA's effect upon the analgesic responses to cold-water swims, 2-deoxy-D-glucose, inescapable foot shock and morphine were determined using the flinch-jump and tail-flick tests. PCPA, which produced an 85% depletion of brain serotonin, significantly decreased jump thresholds while significantly increasing tail-flick latencies. Similarly, while morphine analgesia was decreased by PCPA on the flinch-jump test, it was not affected on the tail-flick test. The analgesic jump thresholds induced by cold-water swims and 2-deoxy-D-glucose as well as the increase tail-flick latencies induced by foot shock were unaffected by PCPA. These results are discussed in terms of PCPA's differential effects upon basal nociception and morphine analgesia and in terms of further dissociation between morphine and stress-induced analgesia.
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PMID:Stress and morphine analgesia: alterations following p-chlorophenylalanine. 645 44

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


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