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At least 955 records · Page 53Linked to original sources
PubMed1983

An assessment of physiological finger tremor as an indicator of beta-adrenoceptor function.

Physiological finger tremor has been assessed as an indicator of beta-adrenoceptor function. Tremor was not correlated with the sex, age, weight or height of the subjects and was stable over 5 min when the hand and fingers were held horizontally. It was not increased by mental arithmetic, the Valsalva manoeuvre or 3 min exercise. Satisfactory dose-response curves could be constructed for the isoprenaline enhanced increases in finger tremor. In six subjects, practolol 120 mg produced a small shift to the right of the isoprenaline dose-response curve for finger tremor (dose ratio 2.1) but propranolol 40 mg was seven times more effective (dose ratio 17.1). Physiological finger tremor appears to be a stable parameter which may be useful in the investigation of the selectivity of beta-adrenoceptor blocking drugs.

Adult↗
PubMed1990

Tremor and the anti-obesity drug BRL 26830A.

The thermogenic beta 3-adrenoceptor agonist BRL 26830A has been shown to increase weight loss in dieting subjects but tremor was a frequent adverse effect. We have investigated the magnitude and nature of this tremor after a single oral dose in 18 subjects. Two complementary techniques were used to attach the recording apparatus to the subjects to give both isotonic and isometric measures of tremor. Increases of 84% and 40% respectively were found due to exaggeration of physiological tremor presumably mediated through concomitant beta 2-adrenoceptor stimulation. The use of beta 3-adrenoceptor agonist drugs in the treatment of obesity may increase but the development of an agent without tremor inducing properties would be an obvious advantage.

Adrenergic beta-Agonists↗
PubMed1985

Effects of p,p'-DDT on the rat brain concentrations of biogenic amine and amino acid neurotransmitters and their association with p,p'-DDT-induced tremor and hyperthermia.

Male, Fischer strain 344 adult rats were given various doses (25-100 mg/kg) of p,p'-DDT by oral gavage, and levels of biogenic amines, their metabolites, and amino acid neurotransmitters, tremor activity, and rectal temperature were measured at several intervals (2, 5, 12, and 24 h) after dosing. Dose-related increases in rectal temperature and in tremor activity were observed at 50-100 mg/kg 12 h after dosing. Tremorigenic doses of DDT increased the 5-hydroxyindoleacetic acid (5-HIAA) level in hypothalamus, brainstem, and striatum, whereas doses of 75 and 100 mg/kg increased the 3-methoxy-4-hydroxyphenylglycol (MHPG) level in hypothalamus and brainstem and the 3,4-dihydroxyphenylacetic acid level in striatum. Six amino acids were assayed in the brainstem, hypothalamus, and striatum; aspartate and glutamate levels were increased only in brainstem at 25-100 mg/kg. No consistent changes in concentrations of taurine, glutamine, glycine, or gamma-aminobutyric acid were observed in any of the regions assayed. Time-related increases in rectal temperature were seen 2-12 h after dosing, and the presence of tremor was observed 5-12 h after dosing; for both the time of peak effect was at 12 h. The DDT-induced hyperthermia and tremor were associated with dose- and time-related increases in levels of 5-HIAA, MHPG, aspartate, and glutamate. It is suggested that an increase in the turnover rate of 5-hydroxytryptamine (5-HT) may be responsible for the DDT-induced hyperthermia, whereas increases in the metabolism of 5-HT and norepinephrine may be involved in the tremor.

Amino Acids↗
PubMed1959

The analysis of drug-induced tremor in mice.

An improved method of recording tremor in mice has been developed using a gramophone pick-up and a cathode ray oscillograph. Permanent records are made on 35 mm. film from which it is possible to determine qualitative differences in the tremor caused by various drugs. In addition, the severity of the tremor may be estimated quantitatively by a tremor index. The rate and variations in the rhythm and amplitude and in the tremor index have been determined for Tremorine (1,4-dipyrrolidin-1'-ylbut-2-yne), harmine, harmaline, 3-amino-1,1,3-triphenylpropan-1-ol and lysergic acid diethylamide. The incidence of side effects has also been noted.

Animals↗
PubMed1986

Central beta-adrenoceptors can modulate 5-hydroxytryptamine-induced tremor in rats.

The effects of two beta 2-adrenoceptor agonists with different lipophilicities were studied on tremor induced by L-5-hydroxytryptophan (L-5-HTP) in pargyline- and carbidopa-pretreated rats. Tremor was recorded and analysed by an objective method based on accelerometry. Clenbuterol, a lipophilic beta 2-selective agonist, dose-dependently enhanced tremor intensity, whereas the hydrophilic beta 2-agonist terbutaline had no effect. The clenbuterol-induced enhancement of tremor was completely abolished by the beta 2-selective antagonist ICI 118,551 but unchanged by the beta 1-selective antagonist metoprolol. The results suggest that centrally located beta 2-adrenoceptors can mediate a modulation of 5-hydroxytryptamine-induced tremor in rats.

5-Hydroxytryptophan↗
PubMed1983

The effect of the GABA-agonist, progabide, on benign essential tremor. A controlled clinical trial.

In a double-blind crossover trial of two 2-week treatment periods, to which 18 patients with benign essential tremor were admitted, there was no statistically significant different between progabide 11.4-20.2 mg/kg X day (median 14.2 mg/kg X day) and placebo in tremor score and tremor amplitude. However, there was a definite placebo and period effect with reduction of tremor score and tremor amplitude during the second period of treatment compared to the first period of treatment, regardless of the treatment regime. This was presumably a result of prolonged treatment and habituation to the test situation and not an effect of the active drug. No side-effects were registered and no laboratory abnormalities were seen.

Adult↗
PubMed1986

Clozapine in the treatment of tremor.

In an open trial 25 tremor patients were treated with clozapine in small doses (18-75 mg per day). The effect was measured with a new movement analyzer. Nine of 12 essential tremor patients were greatly improved. In six of nine patients with Parkinson tremor and in two combined essential tremor/Parkinson tremor patients tremor almost disappeared. Sedation is a major side effect, but decreases in most patients with time. The risk of agranulocytosis makes blood control necessary.

Alcoholism↗
PubMed1985

Beta-adrenoceptor agonists do not cause tremor in the conscious rat.

The ability of some beta-adrenoceptor agonists to induce tremor via skeletal muscle beta 2-adrenoceptors in conscious unrestrained rats has been investigated. Tremor was assessed by visual observation and by an objective method based on accelerometry. Infusion of isoprenaline or terbutaline did not cause tremor, neither did beta-stimulation potentiate an established mild tremor produced by central muscarinic receptor stimulation. Since beta-agonists readily produce tremor in man via skeletal muscle beta 2-adrenoceptor stimulation, our findings indicate that these receptors have a different function in the rat.

Adrenergic beta-Agonists↗
PubMed1987

Blockade of central beta-adrenoceptors attenuates tremor induced by 5-hydroxytryptamine (5-HT)-receptor activation in rats.

The effect of beta-adrenoceptor antagonists, varying in lipophilicity and receptor selectivity, were studied on tremor elicited by L-5-hydroxytryptophan (L-5-HTP) in rats pretreated with a peripherally acting decarboxylase inhibitor and a monoamine oxidase inhibitor, or by the directly acting 5-HT agonist 5-methoxy-N,N-dimethyltryptamine (5-MeODMT). Plasma levels of the beta-adrenoceptor antagonists were determined simultaneously. The non-selective lipophilic adrenoceptor antagonist propranolol was found to dose-dependently reduce tremor intensity, whereas the non-selective hydrophilic adrenoceptor antagonist sotalol had no effect, indicating a central site of action. Furthermore, beta 1-selective blockade with the adrenoceptor antagonist metoprolol had no effect on tremor intensity, whereas the beta 2-selective antagonist ICI 118,551 dose-dependently suppressed tremor intensity, suggesting that the beta-adrenoceptor subtype involved is of the beta 2-type. These results suggest that blockade of centrally located beta 2-adrenoceptors are able to attenuate the tremor response following 5-hydroxytryptamine receptor activation.

5-Hydroxytryptophan↗
PubMed1983

Hand and ECG tremor in spinal muscular atrophy.

The presence of hand and electrocardiogram (ECG) tremor was studied in 31 children with severe, intermediate, or mild form of spinal muscular atrophy. Clinical tremor of the hands was seen in 16 (59%) of 27 patients, all with benign forms of the disease. Nineteen patients had ECG tremors, of whom 17 had the mild or intermediate form. With the exception of one, all patients in the mild or intermediate group had hand or ECG tremor. Hand and ECG tremor are valuable in the diagnosis of the benign forms of spinal muscular atrophy; they are of no value in diagnosis of the severe infantile type.

Adolescent↗
PubMed1974

Correlation between tremor, voluntary contraction, and firing pattern of motor units in Parkinson's disease.

PATIENTS WITH TREMOR OF PARKINSONISM SHOW THREE CHARACTERISTICS OF MOTOR UNIT ACTIVITY: rhythmic spontaneous resting discharge, abnormally low firing rates during voluntary contraction, and consistent differences in firing pattern between small and large motor units. Smaller units discharge once per tremor beat at weak contractions but change into bursts of two or three spikes per beat at stronger forces. Large units are later recruited and fire preferentially once per beat. The large tremor amplitudes can be partly explained by synchronization of unfused twitches of low frequency units which summate more powerfully than the partially fused contractions during physiological tremor, which is about twice as rapid. Tremor is strongly influenced by the force of voluntary contraction. It is strongest at rest or during weak muscular effort and with increasing force becomes continuously of higher frequency and smaller amplitude. Both changes are the consequence of increasing discharge rates of motoneurones at stronger contractions.

Electromyography↗
PubMed1981

Metoprolol and propranolol in essential tremor: a double-blind, controlled study.

Single oral doses of propranolol (120 mg), metoprolol (150 mg) and placebo were given in a randomised, double-blind fashion to 23 patients with essential tremor. Both beta blockers were significantly more effective than placebo in reducing the magnitude of tremor. The decrease in tremor produced by metoprolol (47, sem 9%, n = 23) was not significantly different from that observed propranolol (55, sem 5%, n = 23). Tachycardia on standing was antagonised by both drugs to a similar extent. These findings suggest that metoprolol may represent a valuable alternative to propranolol in the treatment of essential tremor. The data is consistent with the hypothesis that the tremorolytic effect of beta blockers in these patients may be unrelated to peripheral beta-2 adreno-receptor blockade, being possibly mediated by other central or peripheral modes of action of these drugs. However, it cannot be excluded that at the dose used, metoprolol had lost its relative cardio-selectivity and that the reduction in tremor was mediated by competitive antagonism at beta-2 receptor sites in skeletal muscle.

Adult↗
PubMed1984

Adrenergic beta-receptor sensitivity in essential tremor.

Adrenergic beta-receptor sensitivity of six male patients with essential tremor and six age-matched normal controls was assessed by measuring the response in the heart rate and postural tremor to incremental injections of the adrenergic beta-agonist isoprenaline. The relative increase in heart rate and tremor in essential tremor patients did not differ from that in normal controls. It is concluded that no major abnormality is likely to exist in the peripheral adrenergic beta-receptor sensitivity in essential tremor.

Adult↗
PubMed1986

A comparison of primidone, propranolol, and placebo in essential tremor, using quantitative analysis.

The effects of placebo, propranolol and primidone were compared in 14 patients with essential tremor in a double blind, randomised, crossover study. Objective measures of tremor were obtained using an accelerometer with subsequent spectral analysis. Both propranolol (p less than 0.01) and primidone (p less than 0.01) gave significant improvement in tremor, but there was no significant difference in improvement between these drugs. Patients with higher dominant frequencies of tremor tended to respond to both drugs, while those with lower frequencies improved on one or other. There was no differential effect between the drugs with the frequency of tremor.

Clinical Trials as Topic↗
PubMed1987

Stretch reflex oscillations and essential tremor.

Using a computer-controlled torque motor and manipulandum, 50 ms torque pulses and 70 second trains of binary pseudorandom torque disturbances were applied to the wrists of 10 adult controls and 22 patients with essential tremor in order to study the interaction between mechanically-induced stretch-reflex oscillations and essential tremor. These two oscillations were separated by applying inertial and spring loads to the wrist. There was no evidence of increased or unstable stretch-reflex activity in the essential tremor patients, and stretch-reflex latencies did not correlate with the frequency of essential tremor. Essential tremor and mechanically-induced stretch-reflex oscillations are separate phenomena capable of complex interaction.

Adult↗
PubMed1993

Chronic thalamic stimulation improves tremor and levodopa induced dyskinesias in Parkinson's disease.

Chronic thalamic stimulation was performed in 10 Parkinsonian patients with disabling tremor and poor response to drug therapy. During the stereotactic procedure, an electrode was introduced in the ventralis intermediate nucleus of the thalamus. Test stimulation was performed during the intra-operative procedure and a few days after surgery using an external stimulator. When tremor was obviously reduced by thalamic stimulation, an internal stimulator was implanted under the clavicle. Tremor was initially suppressed in all cases and reappeared whenever stimulation was stopped. Patients were followed for 22 to 34 months. Tremor was controlled in eight cases but reappeared after three months in two cases. Levodopa induced dyskinesias were observed before electrode implantation in 5 cases. They consisted of peak-dose choreic or ballistic dyskinesias in 4 cases and biphasic dystonic dyskinesias in 3 cases. Peak-dose dyskinesias were greatly improved or suppressed in all cases. Biphasic dyskinesias were improved in 2 cases. Thalamic stimulation was well tolerated. Mild dystonic hand posture related to the deep brain stimulation was observed in one case. No neuropsychological side-effects were noted. Thalamic stimulation could prove to be an adequate treatment for resistant tremor and levodopa induced dyskinesias.

Aged↗
PubMed1993

Assessing tremor severity.

A clinical rating scale which measured the severity of tremor in 20 patients (12 with essential tremor and 8 with "dystonic" tremor) was assessed at specific anatomical sites for both inter and intra-rater reliability using four raters. The scores obtained with the scale were compared with the results of upper limb accelerometry, an activity of daily living self-questionnaire and estimates of the tremor induced impairment in writing and drawing specimens. The results show that, for the purposes of routine assessment and therapeutic trials, a clinical rating scale can produce reliable results which are a more valid index of tremor induced disability than standard postural accelerometry.

Activities of Daily Living↗
PubMed1995

Exacerbation of postural tremor with emergence of parkinsonism after treatment with neuroleptic drugs.

Neuroleptic medication in three patients with prior isolated postural arm tremor led to a conspicuous deterioration; the postural tremor increased in amplitude, tremor appeared at rest, and other signs of mild parkinsonism developed. Withdrawal of neuroleptic drugs led to improvement in tremor and disappearance of parkinsonism. Positron emission tomography showed no reduction in uptake of [18F]dopa into nigrostriatal terminals suggesting that these patients did not have Parkinson's disease. Neuroleptic drugs can convert postural essential arm tremor into that characteristic of Parkinson's disease in patients with no evident nigrostriatal lesion.

Adult↗