benzofurans has been researched along with Tremor* in 10 studies
1 review(s) available for benzofurans and Tremor
Article | Year |
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[Toxic neurologic manifestations during angina pectoris treatment (perhexiline maleate and amiotadone hydrochloride)].
Topics: Amiodarone; Angina Pectoris; Benzofurans; Cerebrospinal Fluid Proteins; Electromyography; Humans; Inclusion Bodies; Lipid Metabolism; Microscopy, Electron; Movement Disorders; Muscles; Nervous System Diseases; Paresthesia; Perhexiline; Peripheral Nerves; Peripheral Nervous System Diseases; Pigments, Biological; Piperidines; Polyradiculoneuropathy; Schwann Cells; Skin; Tremor | 1978 |
9 other study(ies) available for benzofurans and Tremor
Article | Year |
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Tremetone and structurally related compounds in white snakeroot ( Ageratina altissima ): a plant associated with trembles and milk sickness.
Ingestion of white snakeroot ( Ageratina altissima ) can cause trembles in livestock and milk sickness in humans. The toxicity has been associated with tremetol, a relatively crude, multicomponent lipophilic extract of the plant. In this study, 11 different compounds were isolated from white snakeroot-derived lipophilic extracts from 18 collections. Six of the isolated compounds have not been previously reported to be found in white snakeroot. High-performance liquid chromatography (HPLC) analysis indicated that there are three different chemotypes of white snakeroot from the plant samples analyzed. Elucidation of these chemotypes may explain the sporadic and unpredictable toxicity of white snakeroot to livestock and humans. Topics: Ageratina; Benzofurans; Humans; Milk Sickness; Plant Extracts; Tremor | 2010 |
Effects of chronic discontinuous and continuous treatment of rats with a dopamine D1 receptor antagonist (NNC-756).
Rats were treated intermittently or continuously with the dopamine D1 receptor antagonist NNC-756 for 15 weeks. Two weeks after withdrawal they were challenged with the dopamine D1 receptor agonist SK&F 38393, either alone or after pretreatment with NNC-756. Neither treatment regimen resulted in irreversible increases in oral activities when treated rats were compared with controls; however, transient elevations were observed in the beginning of treatment in the continuously treated group and in the withdrawal phase in the discontinuously treated group. Furthermore, discontinuous treatment resulted in within-group elevations in vacuous chewing movements and tongue protrusions after withdrawal. Dopamine D1 receptor supersensitivity was not observed after challenge with the dopamine D1 receptor agonist. NNC-756 efficiently blocked the behavioural response to stimulation with SK&F 38393. Both treatment regimens resulted in the development of rigidity and catalepsy. The present study suggests that treatment with selective dopamine D1 receptor antagonists is less likely to cause irreversible oral dyskinesia than is treatment with classical neuroleptic drugs. Topics: 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine; Animals; Benzazepines; Benzofurans; Dopamine Antagonists; Drug Administration Schedule; Dyskinesia, Drug-Induced; Face; Jaw; Male; Rats; Rats, Wistar; Tongue; Tremor | 1993 |
Disabling neurological complications of amiodarone.
Five patients developed neurological symptoms during treatment with amiodarone for intervals ranging between five and 40 months. In each case the daily maintenance dose did not exceed 600 mg. The neurological manifestations included gait ataxia, tremor, polyneuropathy, and myopathy. In all five patients, the neurological symptoms were severe and disabling. In one patient with a myopathy, there was no improvement after amiodarone was withdrawn. The neurological side effects of amiodarone may be disabling and are not always reversible with drug withdrawal. Neurological complications may arise during treatment with usual maintenance doses. Topics: Aged; Amiodarone; Benzofurans; Biopsy; Electromyography; Female; Gait; Humans; Male; Muscle Hypotonia; Muscles; Neurologic Examination; Neuromuscular Diseases; Tremor | 1985 |
Frequent neurologic toxicity associated with amiodarone therapy.
Fifty-four consecutive patients were treated with amiodarone for symptomatic ventricular tachycardia or ventricular fibrillation refractory to treatment with conventional antiarrhythmic drugs. A reversible neurologic syndrome of tremor, ataxia, and occasionally peripheral neuropathy without nystagmus, dizziness, encephalopathy, or long-tract signs developed in 54% of the patients and was the most common reason for altering or discontinuing drug therapy. Neurologic side effects improved or resolved within 2 days to 4 weeks of decreasing or discontinuing amiodarone. Frequent neurologic toxicity is a hitherto undescribed complication of amiodarone therapy. Wider recognition of this syndrome will avoid unnecessary and costly diagnostic evaluation. Topics: Amiodarone; Ataxia; Benzofurans; Female; Humans; Male; Middle Aged; Nervous System Diseases; Tremor | 1984 |
Amiodarone neuropathy.
Amiodarone, a drug used to treat refractory cardiac arrhythmias, produced a peripheral neuropathy in 5 of 50 cases (10%). Although the neuropathy may be severe, it tends to improve with lowering of the dosage or discontinuation of the medication. Topics: Aged; Amiodarone; Arrhythmias, Cardiac; Benzofurans; Female; Humans; Male; Middle Aged; Nervous System Diseases; Paresthesia; Peripheral Nervous System Diseases; Tremor | 1983 |
Long-term efficacy and toxicity of high-dose amiodarone therapy for ventricular tachycardia or ventricular fibrillation.
Amiodarone was administered to 154 patients who had sustained, symptomatic ventricular tachycardia (VT) (n = 118) or a cardiac arrest (n = 36) and who were refractory to conventional antiarrhythmic drugs. The loading dose was 800 mg/day for 6 weeks and the maintenance dose was 600 mg/day. Sixty-nine percent of patients continued treatment with amiodarone and had no recurrence of symptomatic VT or ventricular fibrillation (VF) over a follow-up of 6 to 52 months (mean +/- standard deviation 14.2 +/- 8.2). Six percent of the patients had a nonfatal recurrence of VT and were successfully managed by continuing amiodarone at a higher dose or by the addition of a conventional antiarrhythmic drug. One or more adverse drug reactions occurred in 51% of patients. Adverse effects forced a reduction in the dose of amiodarone in 41% and discontinuation of amiodarone in 10% of patients. The most common symptomatic adverse reactions were tremor or ataxia (35%), nausea and anorexia (8%), visual halos or blurring (6%), thyroid function abnormalities (6%) and pulmonary interstitial infiltrates (5%). Although large-dose amiodarone is highly effective in the long-term treatment of VT or VF refractory to conventional antiarrhythmic drugs, it causes significant toxicity in approximately 50% of patients. However, when the dose is adjusted based on clinical response or the development of adverse effects, 75% of patients with VT or VF can be successfully managed with amiodarone. Topics: Aged; Amiodarone; Anorexia; Ataxia; Benzofurans; Female; Heart Arrest; Humans; Lung Diseases; Male; Middle Aged; Nausea; Recurrence; Tachycardia; Thyroid Diseases; Time Factors; Tremor; Ventricular Fibrillation; Vision Disorders | 1983 |
[Amiodarone: review of its antianginal properties and analysis of side effects].
Topics: Amiodarone; Angina Pectoris; Arrhythmias, Cardiac; Benzofurans; Corneal Diseases; Coronary Vessels; Drug Interactions; Humans; Thyroid Diseases; Tremor | 1982 |
Letter: Amiodarone and neurological side-effects.
Topics: Angina Pectoris; Antihypertensive Agents; Ataxia; Benzofurans; Diethylamines; Humans; Hypertension; Iodobenzenes; Male; Paresthesia; Tremor | 1974 |
[Amiodarone and trembling].
Topics: Aged; Antihypertensive Agents; Benzofurans; Coronary Disease; Female; Humans; Male; Myocardial Infarction; Tremor | 1972 |