Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three placebo-controlled double-blind and crossover trials were carried out to analyze the effects of oral yohimbine (YOH) 0.8 mg/kg on mood and performance in 16 healthy students. Subjective assessments (visual analogue scales, side-effects on questionnaire) and objective measurements (digit symbols, flicker fusion, tapping, heterophoria) were done at baseline, and post treatment. YOH shifted the healthy subjects' mood towards feeling panicked, elevated systolic blood pressure and plasma prolactin concentrations, reduced digit symbol substitution, and induced drowsiness and passiveness. Caffeine (CAF) 10 mg/kg raised plasma cortisol and rendered the subjects slightly panicked. Muzziness, clumsiness, tremor, chills and nausea were common after both YOH and CAF. Diazepam (DZ) 0.3 mg/kg given at 60 min antagonized some effects of CAF but failed to antagonize YOH. Clonidine (CLO) 100 micrograms counteracted YOH effects on blood pressure but less the subjective and hormonal effects. CLO 200 micrograms partly antagonized the pressor, sedative but not the hormonal responses of YOH. DZ counteracted YOH effects on plasma cortisol on panic but not on other subjective measures or plasma prolactin. Since CLO did not abolish YOH-induced prolactin increase, it is suggested that these effects of YOH are mediated not only via adrenergic alpha 2-receptors; other mechanisms made important contributions.
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PMID:Anxiogenic effect of yohimbine in healthy subjects: comparison with caffeine and antagonism by clonidine and diazepam. 315 10

Effects of intravenous administration of the serotonin precursor tryptophan (TRP) on serum prolactin, neuromotor function, subjective mood, and blood pressure and pulse were determined in nine depressed patients before and during placebo-controlled treatment with the monoamine oxidase inhibitor (MAOI) tranylcypromine. Tranylcypromine significantly increased the prolactin response to TRP. Four patients developed a distinctive neuromotor syndrome following TRP during tranylcypromine, but not placebo, treatment. Symptoms included hyperreflexia, ankle clonus, nystagmus, incoordination, tremor, myoclonic jerks, and nausea. There were no differences in peak prolactin, mood, or autonomic responses between patients with and without the syndrome, but those with the syndrome had received active tranylcypromine for a significantly shorter duration. Tranylcypromine had little effect on TRP-induced changes in mood or autonomic function, except for a modest enhancement of the TRP-induced rise in diastolic blood pressure. These results suggest that tranylcypromine treatment may enhance serotonin function in depression.
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PMID:Effects of tranylcypromine treatment on neuroendocrine, behavioral, and autonomic responses to tryptophan in depressed patients. 403 56

Metoclopramide antagonizes the effect of dopamine in the central nervous system and other organ systems. Metoclopramide's effect on the medullary chemoreceptor trigger zone makes it useful as a routine anti-emetic and in preventing vomiting induced by antineoplastic drugs, particularly cisplatin. Metoclopramide's gastrointestinal smooth muscle stimulatory effects are related to its ability to antagonize the inhibitory neurotransmitter, dopamine; to augment acetylcholine release and sensitize the muscarinic receptors of the gastrointestinal smooth muscle; and to coordinate gastric-pyloric-small intestinal motor function. The indications for which metoclopramide is approved in the United States are reviewed. Adverse effects, which may occur in up to 20% of patients, include drowsiness, lassitude, and akathisia; all are usually mild, transient, and reversible. Tremor, dystonic reactions, and extrapyramidal effects are infrequent; breast enlargement, galactorrhea, and menstrual irregularities are related to prolactin release.
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PMID:Metoclopramide: pharmacology and clinical application. 633 44

It has recently been demonstrated that human pancreatic GH-releasing factor (hpGRF-44) and Tyr-D-Trp-Ala-Trp-D-Phe-NH2 (subsequently referred to as 'the peptide') release GH from rat pituitary glands maintained in vitro and, in the former case, increase circulating GH in rats and man. The commercial importance of discovering an agent capable of specifically enhancing GH secretion in ruminants stimulated the present study which examined: the intravenous administration of both peptides on plasma GH, prolactin, insulin, glucose, urea and non-esterified fatty acids in goats and the effect of the peptide on the release of GH from sheep pituitary glands maintained in vitro. The peptide was injected into the jugular vein of goats in three different forms and at several concentrations (dispersal by shaking, 0.07 microgram/kg; 0.7 microgram/kg; ball-milled, 7.0 micrograms/kg, 70 micrograms/kg; dimethyl sulphoxide (5%), 7.0 micrograms/kg, 70 micrograms/kg). None of the treatments stimulated a significant increase in circulating GH. Nevertheless the peptide (20 micrograms/ml medium) was found to stimulate a 50-60% increase in the production of GH from sheep pituitary glands maintained in vitro. The effect of intravenously injecting hpGRF-44 (1.0 microgram/kg) was investigated in the present and absence of passive immunization with sheep anti-somatostatin immunoglobulin G (IgG) (a bolus of 600 mg, 3 h before treatment with hpGRF-44). Plasma GH was increased (P less than 0.001) within 15 min of treatment and the magnitude of the response was the same for both the immunized and non-immunized goats. A second peak was measured after approximately 75 min which was only significant (P less than 0.05) in the immunized group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of intravenous administration of growth hormone-releasing factor (hpGRF-44) and Tyr-D-Trp-Ala-Trp-D-Phe-NH2 on plasma hormones and metabolites in goats. 643 24

In previous work, we demonstrated in animals and humans an antidopaminergic effect of estradiol at the level of the striatum. In the present study, we tested the effect of a large dose of estradiol (0.5 mg s.c.) administered either acutely or during several days in four female ovariectomized monkeys, displaying a persistent buccolingual dyskinesia due primarily to a midbrain lesion, but which is markedly enhanced by dopaminergic agonists. One of the monkeys also displayed a lesion-induced parkinsonian-like tremor of the opposite limbs. Chronic administration of estradiol markedly reduced the apomorphine-induced potentiation of the dyskinesia but did not affect the tremor. A single dose of estradiol was followed after 24 h by a 75% reduction of the effect of apomorphine on the dyskinesia but a 50% increase in the response to apomorphine was seen after 2 weeks. The response was at the control level after 30 days. Domperidone, a peripheral dopamine agonist that does not cross the blood-brain barrier and which causes an elevation of prolactin similar to that seen after estradiol, is followed by a similar biphasic modification of the response to apomorphine. Our results suggest that estradiol may have opposite effects on the sensitivity of the striatal dopamine receptors and therefore on dyskinesia, depending on the time of observation. An elevation of prolactin appears to have similar effects. Moreover, some effects of these hormones may be delayed by several days to weeks in primates.
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PMID:Biphasic effect of estradiol and domperidone on lingual dyskinesia in monkeys. 662 6

A 10-day random double-blind study on the effect of bromocriptine versus placebo in severe alcohol-withdrawal symptoms was conducted in 60 alcoholics. The effect of bromocriptine--a dopamine agonist--was significantly better than placebo in ameliorating the following symptoms: anxiety, restlessness, depression, tremor, sweating and nausea as well as the total score of these symptoms. Also in the evaluation of specific symptoms according to a symptom check list of psychiatric, behavioural and social aspects, and in a global evaluation, bromocriptine was clearly superior to placebo. Serum prolactin studied on the first and tenth day of the survey showed a significant increase occurring in the placebo-treated patients. Side effects related to the use of bromocriptine were negligible. Our findings support recent experimental evidence that alcohol-withdrawal symptoms, at least in part, are related to a transient dopaminergic dysfunction in the brain.
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PMID:Bromocriptine in the treatment of the alcohol-withdrawal syndrome. 676 59

We report a 68 year old man with a 7 year history of Parkinson's disease (PD) who obtained little benefit from treatment by dopaminergic and anticholinergic agents. During the six months prior to presentation, he experienced more rapid deterioration in symptoms including memory functions, increasing depression, and dystonia of the foot. External application of picoTesla range magnetic fields (MF) resulted in rapid attenuation of tremor and foot dystonia with improvements in gait, postural reflexes, mood, anxiety, cognitive, and autonomic functions. Plasma prolactin and luteinizing hormone (LH) levels rose three days after initiation of treatment. In addition, distinct electroencephalographic (EEG) changes were recorded nine days after two treatments with MF and included enhancement of alpha and beta activities as well as resolution of the theta activity. These findings demonstrate, for the first time, objective EEG changes in response to picoTesla range MF in PD. Since the pineal gland is a magnetosensor and as some of the clinical effects produced by MF such as relaxation, sleepiness, mood elevation, increased dreaming, and enhancement of alpha and beta activities in the EEG have also been noted in healthy subjects administered melatonin, we propose that the clinical effects as well as the EEG changes noted after treatment with MF were mediated by the pineal gland which previously has been implicated in the pathophysiology of PD.
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PMID:The effects of external picoTesla range magnetic fields on the EEG in Parkinson's disease. 808 28

Kennedy-Alter-Sung (KAS) disease in a hereditary lower motor neuron disease. In this study, we investigate 2 KAS patients presenting with progressive muscle weakness and wasting, action tremor, perioral fasciculation and gynecomastia. Three carriers and 5 healthy members from this 3-generation KAS Chinese family and 60 normal Chinese controls were included in this study. Hormone studies revealed normal serum level in thyrotropin, prolactin, testosterone, leuteinizing hormone, follicle stimulating hormone, and estradiol. Lipid study disclosed type IV hyperlipoproteinemia in 2 KAS patients and 3 healthy members. Molecular studies revealed that the number of CAG triplet repeats in the first exon of androgen receptor gene of the normal allele is in the range of 15-19 and 12-25 in this family and normal controls, respectively. However, the number of CAG repeat of androgen receptor gene were unstable in the mutant alleles with a range of 41-45 and increased from generation to generation (genomic anticipation) in the 2 KAS patients and 3 female carriers. We conclude that the CAG triplet repeats in mutant allele were unstable in the family with the KAS disease. Furthermore, type IV hyperlipoproteinemia may be a co-transmitted syndrome in the family with KAS disease.
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PMID:Type IV hyperlipoproteinemia and moderate instability of CAG triplet expansion in the androgen-receptor gene. Lipid, sex hormone and molecular study in a Chinese family with Kennedy-Alter-Sung disease. 861 Apr 94

In patients with parkinsonism, essential tremor, torsion dystonia, choreic hyperkinesis and hemiballism, a significant increase in the prolactin and thyrotropic hormone was revealed. Possible interrelationship between neuroendocrinological and dysfunction of extrapyramidal structures, is discussed.
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PMID:[The prolactin and thyrotropic hormone content of the blood plasma in neostriatal dysfunction]. 875 36

The effect of repeated cocaine administration on serotonin2 (5-HT2) receptor function was examined in male rats. Rats were fitted with indwelling jugular catheters and subsequently received cocaine (15 mg/kg, i.p., b.i.d.) or saline for 7 days. Rats were challenged with the 5-HT2 agonist DOI (25, 100, 400 micrograms/kg, i.v.) or saline 42 hr and 8 days after cessation of chronic treatment. Serial blood samples were collected at various times after DOI challenge and analyzed for prolactin levels. DOI-induced head shakes and skin jerks were examined concurrently in the same subjects. After 42 hr of withdrawal, the stimulatory effects of DOI on prolactin release and shaking behavior were significantly enhanced in cocaine-treated rats. Conversely, the skin jerk response to DOI was not altered by prior cocaine exposure. After 8 days of withdrawal, the prolactin and head shake responses to DOI were still potentiated in cocaine-treated rats, but this effect was no longer statistically significant. The data indicate that chronic cocaine enhances the sensitivity of 5-HT2 receptor mechanisms. Our findings further suggest the possibility that altered 5-HT2 receptor function may be involved in the mood disturbances experienced by abstinent cocaine addicts.
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PMID:Chronic cocaine exposure potentiates prolactin and head shake responses to 5-HT2 receptor stimulation in rats. 878 4


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