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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ethanol consumption alters the levels and distribution of pantothenic acid and its metabolic products, an effect that can be counteracted by preloading with pantothenic acid. Ethanol also produces significant disturbances in motor function and has a potent tremorolytic activity when administered acutely. To investigate the interaction of pantothenic acid and ethanol, the two substances were administered alone and in combination to three squirrel monkeys trained to perform a response-initiated positioning task that enabled the detection of tremor. Tremor was evaluated using spectral analytical techniques. Ethanol at 1.0 gm/kg produced a tenfold reduction in tremor over control sessions while pantothenic acid alone had no effect on tremor. Pantothenic acid (200 mg/kg, IP or IV) administered before ethanol intubation completely counteracted the tremor-reducing action of ethanol in two monkeys and partially counteracted it in a third. The interaction between pantothenic acid and ethanol was limited to these motor effects; the rate-reducing effect of ethanol was unaffected by pantothenic acid.
J Stud Alcohol 1992 Jan
PMID:Interactions between ethanol and pantothenic acid on tremor and behavior in squirrel monkeys. 155 62

1. Male hooded Lister rats were fed a liquid diet containing 10% absolute ethanol for 4-5 weeks. Control rats received the liquid diet in amounts controlled to produce equal weight gain. 2. The rats were tested 7.5 h after withdrawal of ethanol and 30 min after i.p. injection with nitrendipine, chlordiazepoxide or baclofen or 20 min after i.p. injection with flumazenil. 3. Nitrendipine (25-100 mg/kg) was unable to reverse the anxiogenic responses detected on withdrawal from ethanol, but the highest dose did reduce withdrawal tremor. 4. Chlordiazepoxide (10 mg/kg), flumazenil (4 mg/kg) and baclofen (1.25 mg/kg) significantly reversed the anxiogenic response detected on withdrawal from ethanol. 5. These reversals of ethanol withdrawal responses are similar to the reversal of the increased anxiety detected on withdrawal from chronic treatment with benzodiazepines. 6. The mechanisms and clinical implications of these drug-induced reversals are discussed.
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PMID:Effects of nitrendipine, chlordiazepoxide, flumazenil and baclofen on the increased anxiety resulting from alcohol withdrawal. 155 10

Ethanol (EtOH) withdrawal is characterized by a hyperexcitable state that includes anxiety, tremor, muscle rigidity and seizures. The present three experiments examined the effects of EtOH dependence and withdrawal on the acoustic startle response, an easily quantifiable measure of behavioral reactivity to exteroceptive stimuli. Two intensities of startle stimuli, 105 and 120 dB pulses, were presented to rats during chronic EtOH exposure and during EtOH withdrawal. Prepulse inhibition, which is a sensitive measure of sensorimotor gating processes associated with filtering sensory stimulation, was also assessed during chronic EtOH exposure and withdrawal. Prepulse inhibition was induced by the presentation of a weak 80 dB acoustic stimulus 100 ms prior to a 120 dB stimulus pulse. After 14 days of EtOH liquid diet administration the magnitude of responses elicited by 105 and 120 dB startle stimuli was less in ethanol-treated subjects during continued EtOH access than in animals fed a control liquid diet. When EtOH liquid diet treatment was continued for an additional 3-day period and animals were tested 8 h after withdrawal from EtOH, withdrawn animals were more reactive to startle stimuli at both intensities than were animals maintained on the EtOH liquid diet. A time-course experiment with repeated startle testing at 4, 8, and 12 h post-EtOH exposure revealed significant increases in responding to the 105 dB startle intensity at 8 h post-EtOH exposure. The ability of animals to respond to a prepulse stimulus was not affected during chronic EtOH treatment, but was reduced during withdrawal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responding to acoustic startle during chronic ethanol intoxication and withdrawal. 157 Mar 82

Limited toxicity information is available in the medical literature on the antidepressant fluoxetine (Prozac, Dista Products Co, Indianapolis, IN). The goal of this prospective multicenter study was to develop a toxicity profile of initial signs and symptoms observed in an acute fluoxetine overdose. A prospective study was made of patients reported to one of four American Association of Poison Control Centers' regional poison control centers after ingesting an acute overdose of fluoxetine. A standard data collection form was used on all patients ingesting fluoxetine. Information obtained included age, current medications, dose, coingested drugs, presenting symptoms, vital signs, electrocardiogram abnormalities, outcome, and fluoxetine levels. The authors collected 272 cases; 234 cases met the criteria of the study. Fluoxetine was ingested alone in 87 cases and with ethanol or other drugs in the remaining 147 cases. Of the 87 cases where fluoxetine was ingested alone, 67 patients were adults and 20 were children. Symptoms that were seen in the adult group included: tachycardia (15/67), drowsiness (14/67), tremor (five/67), vomiting (four/67), or nausea (four/67). Thirty patients did not develop symptoms. Twelve of the adult overdose patients had total fluoxetine levels ranging from 232 to 1390 ng/mL. The authors conclude that symptoms that develop after an acute overdose of fluoxetine appear minor and of short duration. Aggressive supportive care is the only intervention necessary.
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PMID:Acute fluoxetine overdose: a report of 234 cases. 158 2

1. Ethanol-induced sleep time was significantly longer in F344 than LEW rats. However, there is no difference in barbital-induced sleep time between F344 and LEW. 2. Development of tolerance to ethanol-induced motor impairment was slightly faster in F344 than in LEW rats. While, LEW rats more easily developed tolerance to the impairment by barbital in comparison with F344 rats. 3. F344 and LEW rats were chronically treated with liquid diet containing ethanol or with barbital-admixed food. After the termination of ethanol and barbital treatments, various withdrawal signs occurred in F344 rats, including tremor and convulsions, whereas LEW rats showed no convulsions. Withdrawal scores of ethanol and barbital were significantly higher in F344 than in LEW rats. 4. These results suggest that strain differences in physical dependence on ethanol and barbital may be mainly influenced by the susceptibility to ethanol and the development of tolerance to barbital, respectively.
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PMID:Susceptibility to, tolerance to, and physical dependence on ethanol and barbital in two inbred strains of rats. 159 18

The effects of alprazolam 1 mg both alone and in combination with 0.5 g/kg of alcohol were examined on self-ratings of intoxication and measures of central and peripheral activity such as EEG, auditory evoked response, tremor at 90, 150 and 210 min post drug. Forty-eight healthy volunteers were assigned randomly to 4 independent groups who received: alprazolam and placebo drink, alprazolam and alcohol, placebo capsule and alcohol, placebo capsule and placebo drink respectively. Alprazolam decreased the amplitudes of the 3 potentials of the evoked response, decreased activity in the 8-13 Hz and increased activity in the 13.5-26 Hz wavebands of the EEG and decreased the frequency at which fusion was perceived. Alcohol prolonged reaction time and increased tremor. The effects were not always additive and alprazolam was dominant in the combination.
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PMID:The effects of alprazolam alone and combined with alcohol on central integrative activity. 160 95

Aqueous gels of two analogous, water-insoluble copolymers A and B have been formed by addition of excess water to concentrated ethanol solutions of the polymers. A and B differed only in their content of cationic groups in a ratio 2:1 (A:B). The gels were converted permanently to fluids (i.e. gel-sol transformation) at high shear rates. Stability of the resulting polymer dispersions depended on the presence and mutual repulsion of the polymer cations. Polymer B dispersions were less stable to the flocculating effect of an electrolyte (sodium chloride). At certain critical concentrations, 0.2 M NaCl (for polymer A), or 0.1 M NaCl (for polymer B) the electrolyte flocculated the otherwise stable dispersions to a gel structure. The electrolyte-flocculated gels were readily redispersed to fluids by shaking but reverted to gels on standing (thixotropic). In contrast the original coacervated gels (without electrolyte) could not be redispersed easily with manual shaking. Lower polymer-polymer interaction in the thixotropic system relates possibly to increases in particle size and irregularity of particle shape during flocculation.
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PMID:Thixotropic phenomenon in flocculated aqueous dispersions of acrylate methacrylate copolymers. 167 78

Hypoglycaemia is possibly the most frequent metabolic emergency, in that insulin-induced hypoglycaemia is a common side-effect of treatment of a common disease. The symptoms are partly sympathetic and related to the release of catecholamines. These symptoms include sweating, tremor, palpitations, sensation of hunger, restlessness and anxiety. Other symptoms are caused by an insufficient supply of glucose to the brain, resulting in neuroglucopenia with symptoms like blurred vision, weakness, slurred speech, vertigo and difficulties in concentration. Symptom recognition is the primary and most effective defence against cerebral dysfunction which is the ultimate consequence of hypoglycaemia. Even in insulin-treated diabetic patients symptom failure might occur. Patients who experience severe episodes of hypoglycaemia do not constitute a special subgroup of patients. However, near-normalization of blood glucose levels have resulted in an increase in the incidence of severe hypoglycaemia. Moreover, the threshold for hormonal counter-regulatory responses in adrenaline, growth hormone and cortisol is lowered after a period of strict metabolic control in insulin-dependent diabetic patients. The glucose level at which the patients become subjectively aware of hypoglycaemia is correspondingly reduced. Other reasons for hypoglycaemia to occur are oral hypoglycaemic agents, especially sulfonylureas which may be potentiated by other drugs. Prolonged hypoglycaemia may be seen after first-order sulfonylureas, and may indicate glucose infusion as treatment. Next to insulin and sulfonylurea, ethanol is the most common cause of hypoglycaemia. In non-diabetics, hypoglycaemia will typically develop 6-24 h after a moderate or heavy intake of ethanol by a person who has had an insufficient intake of food for 1 or 2 days. Insulin-producing tumours, insulinomas and non-islet cell tumours may also be reasons for hypoglycaemia in non-diabetics. Treatment of mild episodes of hypoglycaemia is intake of fast-absorbing carbohydrates. Severe episodes can be treated with either i.v. dextrose or glucagon injected i.m. or i.v. The glycaemic response and recovery of a normal level of consciousness is 1-2 min slower after glucagon than after glucose.
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PMID:Endocrine emergencies. Hypoglycaemia. 173 95

Sertraline is slowly absorbed after oral administration, with peak plasma concentrations at 6-8 h. Plasma concentrations are linearly related to dose. The elimination half-life is about 32 h; metabolism is by demethylation to an inactive metabolite. Once-daily dosing is recommended, with steady state being reached after about 7 days. The kinetics of sertraline in the elderly and in patients with renal impairment are similar to those in young healthy female volunteers. In young male volunteers, peak plasma concentrations were lower, and elimination half-life shorter, than in elderly men or both groups of women. Nevertheless, no reduction in dosage is recommended for these groups. Sertraline is highly active in animal models of depression, and administration of the drug to healthy human beings causes a selective, dose-related inhibition of 5-hydroxytryptamine (5-HT) uptake into blood platelets. Single doses of sertraline in volunteers caused changes in the quantitative pharmaco-electroencephalogram suggesting antidepressant and anxiolytic actions, with sedative potential evident only at doses of 200 mg or more. Sertraline does not impair psychomotor performance, including simulated car driving, and overall seems neither stimulating nor sedating: an increase in critical flicker fusion threshold suggests a slight alerting effect, whereas subjective tests indicate an increase in perceived sedation at doses of 100 mg or more. No potentiation of the effects of ethanol has been noted in either young or elderly subjects. No adverse effects on the electrocardiogram, blood pressure, or systolic time intervals have been detected, and sertraline lacks anticholinergic action. These studies imply a low probability of adverse central nervous and cardiovascular effects. Sertraline is probably a weak inducer of hepatic microsomal enzyme activity. Sertraline does not affect the clearance of lithium but there may be a pharmacodynamic interaction which leads to increased tremor when the drugs are given together. No clinically relevant effects were noted in the interaction studies with digoxin, atenolol and diazepam. The pharmacokinetics and pharmacodynamics of sertraline are generally favourable. However, caution is needed when sertraline is given to patients receiving lithium or drugs with a low therapeutic ratio, such as corticosteroids, oral hypoglycaemic agents, and warfarin.
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PMID:Clinical implications of the pharmacology of sertraline. 180 26

The effects of some tremor-producing and antitremor agents on the enzymes sequentially metabolizing ethanol and acetaldehyde in addition to biogenic-amine-derived aldehyde intermediates were studied in mouse liver preparations. Aldehyde but not alcohol dehydrogenase was differentially stimulated by the compounds studied in vitro. This effect was confined to the mitochondrial enzyme and was isoenzyme-dependent. The results indicate difference between in vitro and in vivo effects and suggest a role for mitochondrial aldehyde dehydrogenase in metabolic detoxification of endogenous biogenic aldehydes in the presence of alcohol which may explain the worsening of drug-induced tremor by ethanol.
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PMID:Effect of tremorogenic and antitumor agents on enzymes regulating a minor metabolic pathway of biogenic amines: an hypothesis for the underlying mechanism. 182 23


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