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)

Many studies cite no more than 80% incidence of hand tremor during withdrawal in known alcoholics, although this symptom is one of the diagnostic signs of addiction. We found that of 48 patients tested, hand tremor increased in 29 Ss after the application of a passive relaxation technique while it decreased in 28. It was found that MMPI data obtained for both groups fitted the inverted U curve in that the most distressed Ss tremored as little as did the least distressed originally, while the tremor increased in the high stress group after relaxation therapy while it decreased in the least stressed group. Implications for alcoholism research and theory were discussed, and the possible superiority of the CES to drug therapy for withdrawal was noted.
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PMID:A curvilinear relationship between alcoholic withdrawal tremor and personality. 37 Jan 54

A 55-year-old man with addiction of alcohol was admitted to our hospital with hematoemesis. After admission, the rupture of esophageal varices was observed and it was treated with endoscopic injection sclerotherapy. On the 3rd hospital day, the patient showed alcohol withdrawal syndrome and therefore haloperidol was administered intramuscularly and intravenously. After a half day of this treatment, high fever, diaphoresis, hypotension, tachycardia, muscular rigidity and tremor developed. With the laboratory data including high serum levels of CK, LDH, GOT and GPT, neuroleptic malignant syndrome (NMS) was suspected. Regardless of intensive care, hepatic failure, DIC and acute renal failure promptly developed, and he died on the 11th hospital day. Neuroleptics may cause serious side effects, such as NMS, when the physical status of patients was deteriorated. Especially in exhausted patient such as our case, even the small dose of neuroleptics caused NMS within short term. Thus, it seemed to be important for clinicians to pay attention to choice of neuroleptics.
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PMID:[A case of neuroleptic malignant syndrome developed in liver cirrhosis patient addicted to alcohol]. 177 76

Some histamine H1 (tripelennamine, diphenhydramine and cyclizine) and H2 (ranitidine and cimetidine) antagonists (1 and 10 mg/kg) were administered to morphine-dependent mice to evaluate the changes on naloxone-induced abstinence syndrome. When antihistaminics were administered 30 min before naloxone (1 mg/kg) on day 4 of morphine addiction, the two doses of three H1 antagonists and the higher dose of ranitidine inhibited shaking behavior. Furthermore, the two doses of tripelennamine and the higher dose of diphenhydramine, cyclizine and cimetidine enhanced jumping behavior. When antihistaminics were administered chronically (during the 4 days of morphine addiction), tripelennamine, cyclizine and ranitidine (all at 10 mg/kg) inhibited shaking behavior. The three H1 antihistaminics used enhanced the number of jumps per mouse whereas ranitidine decreased this response. No significant changes were found in the rest of the withdrawal symptoms after the antihistaminics were administered. The participation of serotonergic and catecholaminergic mechanisms is discussed.
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PMID:Effects of antihistaminics on naloxone-induced withdrawal in morphine-dependent mice. 197 46

1. Doses of buprenorphine (0.01, 0.1, 0.5, 1, 5, 10 and 50 mg/kg) were administered to determine buprenorphine's ability to precipitate abstinence symptoms in morphine-dependent mice. 2. When buprenorphine was administered in the fourth day of morphine addiction, the results demonstrate that the administration of the partial agonist opioid produce a bell-shaped dose-response curve. 3. The highest dose (50 mg/kg) was partially inactive while lower doses causing similar percentage than group treated with naloxone with respect to the appearance of the most of the symptoms of abstinence studied (diarrhoea, tremor, shaking-"wet dog shakes"-, jumping and weight loss). 4. Our findings demonstrate the bell-shaped response curve of the antagonist effects of buprenorphine.
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PMID:Buprenorphine: bell-shaped dose-response curve for its antagonist effects. 205 24

According to the hypothesis that the development of physical dependence on and tolerance to opiates depends on the inhibition by opiates of L-asparaginase and L-glutaminase activities in the brain, and the blockade by opiates of the aspartatergic/glutamatergic receptors especially NMDA, four female and fourty-four male heroin addicts were included in a double-blind clinical trial. Four mg chlorpromazine (CPZ) was administered every hour and 10 mg diazepam (DIA) every 6 hours to a group consisting of two female and nineteen male inpatients. The remaining subjects received 15 mg non-opioid antitussive dextromethorphan (DM) instead of CPZ. The withdrawn addicts were controlled twice a day and yawning, lacrimation, rhinorrhoea, perspiration, goose flesh, muscle tremor, dilated pupils, anorexia, joint and muscle aches, restlessness, insomnia, emesis, diarrhea, craving and rejection of smoking as abstinence syndrome signs were observed and rated on a scale of 1, 2 and 3 points according to their intensity. All signs, except perspiration and emesis, were significantly less intense in the group given DM + DIA than CPZ + DIA. The other plus points included the immediate stop of craving and the early onset of smoking in DM + DIA group. The results are considered to be supporting evidence for the hypothesis emphasizing the blockade of NMDA receptors by opiates in opiate addiction. Furthermore, the decrease caused by non-opioid NMDA antagonists in the responsiveness of NMDA receptors appears very promising for the treatment of opiate addicts.
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PMID:The treatment of heroin addicts with dextromethorphan: a double-blind comparison of dextromethorphan with chlorpromazine. 218 2

Previous research has demonstrated response differences following administration of alcohol between adult males with a positive (FHP) versus negative (FHN) family history of alcoholism. These response differences are thought to reflect differences in vulnerability to dependence on alcohol. Thus, the role of positive family alcoholism history in increasing risk of addiction to a variety of drug classes might be studied by determining whether FHP subjects show different responses to drug classes other than alcohol. This was done in the present study by determining dose-effect functions for a variety of physiological (heart rate, skin conductance, skin temperature), subjective (analog mood and drug effect, Subjective High Assessment Scale), and psychomotor measures (hand tremor, body sway, Digit Symbol Substitution Test, eye-hand coordination, and numeric recall) in FHP and FHN college-aged males for secobarbital (0, 100, 200 mg by mouth) and ethanol (1 g/kg). FHP and FHN subjects were matched on light-to-moderate drinking patterns, anthropometric dimensions, age, years of schooling, and drug use. At equivalent blood alcohol levels family-history positive subjects reported greater effects of ethanol than did family-history negative subjects on almost all subjective measures. Following the high dose of secobarbital, FHP but not FHN subjects showed elevated subjective effects; these effects were substantially less and were evident in fewer measures than following ethanol. In contrast to effects on the subjective measures, ethanol and secobarbital produced comparable impairment in both groups of subjects for most psychomotor responses. Group differences were not obtained on any physiological measures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alcohol and secobarbital effects as a function of familial alcoholism: acute psychophysiological effects. 226 98

The paper provides a survey of neuropharmacological fundamentals for the use of beta-adrenolytics in the treatment of psychiatric and neurological diseases. In particular there are discussed results of animal- and clinical-pharmacological experiments carried out in order to assess the influence of betaadrenolytics in disorders and diseases such as anxiety, psychoses, tremor, some kinds of addiction, migraine and epilepsy. The conclusion is that in spite of some ascertained clinical indications on the one hand and a variety of neuropharmacological results on the other the mode of action of betaadrenolytics at the level of the CNS remains still insufficiently explainable.
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PMID:[The neuropharmacology of beta adrenolytics]. 286 12

Alcohol transiently improves the shakiness of patients with essential (familial) tremor. The possibility that essential tremor may lead to alcohol abuse and addiction is raised in relationship to three case reports. It is suggested that secondary alcoholism in patients with essential tremor may be treated or prevented by control of the essential tremor with beta-adrenergic blocking agents. Theoretical implications for the etiology of alcoholism are discussed.
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PMID:Alcoholism secondary to essential tremor. 706 49

Physiological dependence on benzodiazepines is accompanied by a withdrawal syndrome which is typically characterized by sleep disturbance, irritability, increased tension and anxiety, panic attacks, hand tremor, sweating, difficulty in concentration, dry wretching and nausea, some weight loss, palpitations, headache, muscular pain and stiffness and a host of perceptual changes. Instances are also reported within the high-dosage category of more serious developments such as seizures and psychotic reactions. Withdrawal from normal dosage benzodiazepine treatment can result in a number of symptomatic patterns. The most common is a short-lived "rebound" anxiety and insomnia, coming on within 1-4 days of discontinuation, depending on the half-life of the particular drug. The second pattern is the full-blown withdrawal syndrome, usually lasting 10-14 days; finally, a third pattern may represent the return of anxiety symptoms which then persist until some form of treatment is instituted. Physiological dependence on benzodiazepines can occur following prolonged treatment with therapeutic doses, but it is not clear what proportion of patients are likely to experience a withdrawal syndrome. It is also unknown to what extent the risk of physiological dependence is dependent upon a minimum duration of exposure or dosage of these drugs. Withdrawal phenomena appear to be more severe following withdrawal from high doses or short-acting benzodiazepines. Dependence on alcohol or other sedatives may increase the risk of benzodiazepine dependence, but it has proved difficult to demonstrate unequivocally differences in the relative abuse potential of individual benzodiazepines.
Addiction 1994 Nov
PMID:The benzodiazepine withdrawal syndrome. 784 56

Whereas early formulations of addictive behaviour placed great emphasis upon withdrawal as a defining feature, current views focus more upon compulsive use as its central characteristic. However, the withdrawal syndrome continues to occupy an important place in the study of the addictions. It is interesting both in its own right and in relation to the development and maintenance of the compulsive use of drugs. Despite the attention devoted to withdrawal phenomena over many years, precise demarcation of the withdrawal symptoms associated with drugs of dependence has proved difficult to achieve. Withdrawal from all drugs of dependence appears to lead to mood disturbances although the extent to which these are due to the pharmacological actions of the drugs or to other physiological or psychological processes is unclear. Sleep disturbance is also common, although again direct links with the pharmacological actions of the withdrawn drug are yet to be established. Withdrawal from alcohol, benzodiazepines and opiates is often associated with somatic symptoms. In the former two cases, these can involve sweating, tremor and occasionally seizures. Perceptual disturbances have also been reported. In the case of opiates, flu-like symptoms are often reported, including muscle aches and gastric disturbances. In the case of nicotine, heightened irritability has been established as a direct pharmacological withdrawal effect. Characterization of stimulant withdrawal is still uncertain. There is little evidence of somatic symptoms but depression may occur as a result of a physiological rebound. There is also uncertainty over what role pharmacological withdrawal symptoms play in maintaining compulsive use.(ABSTRACT TRUNCATED AT 250 WORDS)
Addiction 1994 Nov
PMID:Overview: a comparison of withdrawal symptoms from different drug classes. 784 60


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