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

Hyperventilation may be induced by several organic factors. The HVS-hyperventilation and symptoms such as hypertonia and pain-hypocapnia and disturbance of the acid-base balance--other symptoms--anxiousness--hyperventilation--etc. In the adaptation-hyperventilation and symptoms such as hypertonia and pain,-hupocapnia and disturbance of the acid-base balance-other symptoms--anxiousness--hyperventilation--etc. In the adaptation process one distinguishes the load, the strain and a tension or counterforce (stress). In the cause and effect relationship between the adaptation process and a specific pathology, it is obvious that the strain is the only element capable of eliciting the specific pathology or syndrome. Stress is a compensation for the strain and is therefore beneficial to the organism. The strain is associated with, amongst other things, anxiety and changes in the pyridoxine-L-tryptophan metabolism (nicotinic acid-ribonucleotide synthesis). Stress depends to a large extent on the intact serotonergic transmission in the cerebrum. But serotonin synthesis is critically dependent on the pyridoxine-L-tryptophan metabolism. Benzodiazepines improve the hyperventilation, anxiousness and strain, if these are of the free-floating anxiety type. Tricyclic preparations improve anxiousness in as much as it assumes the character of fear, phobia or an anxiety attack. They are active against strain when that reveals itself as an anxiety attack. Pyridoxine and L-tryptophan as serotonergic agonists, improve the hyperventilation, have a beneficial effect on symptoms such as hypertonia and pain, are effective against anxiousness and anxiety and potentiate the stress. In addition they directly correct the property of strain, i.e. the disturbance of the nicotinicacid-ribonucleotide synthesis. Clomipramine is the most potent serotonergic agonist available. That substance has a favourable effect on hyperventilation, hypertonia and pain, on anxiousness that expresses itself as fear, phobia or an anxiety attack. It favours stress. Further investigation is desirable, in particular of the new serotonergic agonists that have recently been made available or are still to come.
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PMID:[Pharmacotherapy of the hyperventilation syndrome]. 614 57

The synthesis of neurotransmitter amines in mammalian brain is known to respond to changes in precursor availability. After dietary manipulation including L-tryptophan supplementation 3 subjects out of 11 showed a significant reduction of experimentally induced ischemic pain. It is suggested that dietary manipulation aimed at an increase in central nervous system serotonin can alter pain perception in some individuals.
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PMID:Effect of L-tryptophan supplementation on ischemic pain. 614 10

The direct electrical stimulation (with biphasic pulses of 1 msec, 10 pulses/sec, 200 microA, for 30 min) of the nucleus raphe magnus in chloral hydrate anaesthesized rats produced a significant acceleration (+50%) of 5-HT synthesis in the spinal cord as revealed by the increased rate of 5-HTP accumulation occurring at this level after the blockade of central 5-HTP decarboxylase with benserazid. In contrast, no change was detected in 5-HT metabolism in the forebrain of stimulated rats. The acceleration of 5-HT synthesis was likely not due to an increased availability of tryptophan for the rate-limiting enzyme, tryptophan hydroxylase, since the concentration of this amino acid was changed neither in the spinal cord, nor in the forebrain of stimulated rats. The measurement of tryptophan hydroxylase activity in soluble extracts from the spinal cord of control and stimulated rats revealed that the acceleration in 5-HT synthesis produced by the electrical stimulation of the nucleus raphe magnus was not associated with a persisting activation of this enzyme. Although one cannot completely exclude that a short-lasting activation of tryptophan hydroxylase, no longer detectable in soluble extracts, has occurred in the spinal cord of stimulated rats, the present findings rather suggest that the rate of 5-HT synthesis can be controlled by factors other than only the concentration of tryptophan and the intrinsic activity of tryptophan hydroxylase in serotoninergic neurons. The demonstration of an acceleration of 5-HT synthesis in bulbospinal serotoninergic neurons under stimulating conditions close to those producing analgesia in rats further supports the role of these neuronal systems in the physiological mechanisms of pain control.
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PMID:Electrical stimulation of the nucleus raphe magnus in the rat. Effects on 5-HT metabolism in the spinal cord. 615 75

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


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