Depression of essential tremor by alpha-adrenergic blockade.

Mai, Jesper; Olsen, Rolf Bang

doi:10.1136/jnnp.44.12.1171

Cited by 15 publications

(9 citation statements)

References 3 publications

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“…Blockade of cx-adrenoceptor sites has been associated with depression of physiological tremor (Mai & Olsen, 1981). In the present study tremor was not changed following acute and chronic administration of alfuzosin.…”

Section: Systolicsupporting

confidence: 48%

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Effect of acute and chronic oral administration of alfuzosin on baroreflex function and tremor in man.

Deering¹,

Riddell²,

Harron³

et al. 1988

Brit J Clinical Pharma

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1. The effects of the acute and chronic administration of the alpha 1‐ adrenoceptor antagonist alfuzosin (5 mg twice daily for 7 days) on baroreflex function, physiological tremor and sedation (visual analogue scale) were investigated in six healthy volunteers. 2. Phenylephrine‐ systolic pressure dose‐response curves were shifted (P less than 0.05) to the right by alfuzosin compared with placebo on day 1, and on day 8 prior to the administration of alfuzosin indicating significant alpha‐ adrenoceptor blockade over 24 h with 5 mg twice daily administration. 3. Baroreflex sensitivity (delta R‐R ms mmHg‐1 systolic arterial pressure) was reduced (P less than 0.05) by alfuzosin compared with placebo on day 1 (13.8 +/‐ 2.6 vs 20.6 +/‐ 3.6 ms mmHg‐1) and on day 8 (13.4 +/‐ 1.7 vs 21.1 +/‐ 2.7 ms mmHg‐1). 4. Maximum power (microV2) or frequency (Hz) of physiological tremor did not change 2 h after alfuzosin administration on day 1 (13.7 +/‐ 4.4 microV2, 9.2 +/‐ 0.3 Hz) or day 8 (11.5 +/‐ 4.3 microV2, 10.0 +/‐ 0.4 Hz) compared with placebo on day 1 (16.9 +/‐ 7.5 microV2, 10.0 +/‐ 0.4 Hz) and day 8 (17.3 +/‐ 5.7 microV2, 10.2 +/‐ 0.8 Hz). 5. Alfuzosin 5 mg twice daily did not cause sedation on day 1 or day 8. 6. In conclusion the reduction in baroreflex sensitivity with the alpha‐adrenoceptor antagonist alfuzosin may contribute to its antihypertensive activity in reducing the reflex tachycardia associated with its hypotensive action.

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Section: Systolicsupporting

confidence: 48%

“…As sedation has been reported with indoramin (Lewis et al, 1973;Fitzgerald, 1981;Deering et al, 1986) and as oaadrenoceptor antagonists may influence tremor (Mai & Olsen, 1981), the effects of alfuzosin on sedation and physiological tremor were also investigated.…”

Section: Introductionmentioning

confidence: 99%

Effect of acute and chronic oral administration of alfuzosin on baroreflex function and tremor in man.

Deering¹,

Riddell²,

Harron³

et al. 1988

Brit J Clinical Pharma

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“…The cause of physiological tremor is thought to be due to oscillations in the gamma loop servomechanism of the spinal stretch reflex. As centrally acting a2-adrenoceptor agonists reduce sympathetic outflow (Kobinger, 1978) and as the a-adrenoceptor antagonist thymoxamine reduced essential tremor via a central mechanism (Mai & Olsen, 1981), the effects of the centrally acting a2-adrenoceptor agonists clonidine and azepexole on tremor are of interest. Neither of these centrally acting agonists influenced physiological tremor significantly.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, indicate that azepexole significantly reduces clonidine facilitates the vagally mediated baro-systolic and diastolic blood pressure in the supine receptor reflex in animals (Kobinger & Walland, and standing position without effect on heart 1971,1972) and in man (Sleight & West, 1975;rate; associated with these cardiovascular effects Guthrie & Kotchen, 1983). Recently the a2-is a significant reduction in plasma noradrenaline adrenoceptor agonist azepexole (B-HT 933) has levels (Rubin et al, 1982 Building, 97 Lisburn Road, Belfast BT9 7BL study was to investigate the effects of azepexole on the baroreceptor mediated reflexes following intravenous boluses of phenylephrine and the Valsalva manoeuvre; and as a-adrenoceptor antagonists are thought to reduce essential tremor via a central mechanism (Mai & Olsen, 1981), its effects on physiological tremor were also investigated. The effects of azepexole were compared with clonidine and placebo.…”

Section: Introductionmentioning

confidence: 99%

Effects of azepexole and clonidine on baroreceptor mediated reflex bradycardia and physiological tremor in man.

Harron¹,

Riddell²,

Shanks³

1985

Brit J Clinical Pharma

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1 The effects of oral administration of axepexole 10 mg, clonidine 300 ,ug and placebo on baroreceptor mediated reflex bradycardia and physiological tremor were investigated in six healthy volunteers. 2 Both azepexole and clonidine reduced (P < 0.05) systolic (120.5 ± 2.5 to 105.0 + 3.3 mm Hg; 115.8 + 2.6 to 104.7 + 2.8 mm Hg respectively) and diastolic (52.5 + 2.6 to 47.2 + 1.4 mmHg; 53.7 + 1.6 to 49.0 ± 1.5 mmHg respectively) pressure when compared to placebo and to pre-treatment values. This reduction in pressure was not accompanied by a change in heart rate. 3 Both azepexole and clonidine enhanced (P < 0.05) baroreflex sensitivity to increases in systolic arterial pressure with phenylephrine. 4 Clonidine facilitated (P < 0.05) baroreflex sensitivity during the strain phase of the Valsalva manoeuvre, whereas azepexole reduced it (P < 0.05). 5 Neither clonidine nor azepexole altered finger tremor when compared to placebo or pre-treatment values. 6 Azepexole produced (P < 0.05) sedation compared to placebo but not when compared to pre-treatment values. Clonidine caused significant increases in sedation when compared to both placebo and to pre-treatment values. 7 The differences between azepexole and clonidine may be due to the greater specificity of azepexole for the a2-adrenoceptor than clonidine.

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“…23 Positron emission tomography [24][25][26] and functional magnetic resonance imaging 27 studies suggest that ET is associated with an abnormal overactivity of cerebellum and connected nuclei (red nucleus and thalamus). 33 Clozapine exhibits potent alpha-1 and alpha-2 adrenergic antagonistic activity in vitro. 28,29 The pharmacodynamics behind clozapine's efficacy on ET are unknown.…”

Section: Discussionmentioning

confidence: 99%

Acute and chronic effects of clozapine in essential tremor

et al. 1999

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Patients with essential tremor (ET) may not respond to commonly used drugs. Clozapine, an atypical neuroleptic drug, has been reported to improve postural Parkinson's disease tremor clinically resembling ET. The effects of a single dose of 12.5 mg clozapine and placebo were evaluated in a randomized, double‐blind, crossover study in 15 drug‐resistant patients with ET. Patient responders with more than 50% improvement after a single dose of clozapine subsequently received the drug (39 ± 9 mg up to 50 mg) unblinded for a period of 15.8 ± 7.7 months. Tremor was effectively reduced by a single dose of clozapine in 13 of 15 patients (p <0.01). Sedation was the only side effect reported during the clozapine test; however, the time course of sedation and of the antitremor effect were not coincident. A significant reduction of tremor was reported with chronic clozapine treatment (p <0.01) with no tolerance to drug antitremor effect, whereas sedation markedly decreased after 6–7 weeks of therapy. No clozapine‐induced hematologic side effects were observed in our cohort of patients during long‐term treatment. Our results suggest that in selected drug‐resistant ET cases, clozapine should be considered before resorting to neurosurgical options.

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Depression of essential tremor by alpha-adrenergic blockade.

Cited by 15 publications

References 3 publications

Effect of acute and chronic oral administration of alfuzosin on baroreflex function and tremor in man.

Effect of acute and chronic oral administration of alfuzosin on baroreflex function and tremor in man.

Effects of azepexole and clonidine on baroreceptor mediated reflex bradycardia and physiological tremor in man.

Acute and chronic effects of clozapine in essential tremor

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