Effect of adrenaline, noradrenaline, atropine, and nicotine on some types of human tremor.

Marshall, John K.; Schnieden, H.

doi:10.1136/jnnp.29.3.214

Cited by 75 publications

(29 citation statements)

References 6 publications

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“…A paradoxical response to anticholinergics cannot easily be explained, but it is not unrecognized. Thus, Marshall and Schnieden (1966) demonstrated that the tremor of Parkinsonism was increased by intravenous atropine. Certainly such a response is an argument against the routine prophylactic use of anticholinergics with antipsychotic drugs.…”

Section: Discussionmentioning

confidence: 98%

Extrapyramidal effects of neuroleptics.

Korczyn¹,

Goldberg²

1976

Journal of Neurology, Neurosurgery & Psychiatry

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SY N OP S I S A study was conducted on 66 psychiatric inpatients who took major tranquilizers for periods of four to 16 years. The frequency of signs of Parkinsonism and the effects of orphenadrine on these were studied in a double-blind crossover method. Sixty-one per cent of the patients showed signs of Parkinsonism. Female patients and those with organic brain pathology more frequently exhibited Parkinsonism (although the difference was not statistically significant). No correlation was found between duration of treatment and extrapyramidal effects. Of the 40 patients who developed Parkinsonism, 25 responded favourably to orphenadrine, while six (15%) had more marked manifestations on orphenadrine than on placebo.Although phenothiazines have been widely used in psychiatry for approximately 20 years, there is relatively little information concerning many aspects of their chronic administration. The recognition of persistent orofacial dyskinesia as a syndrome connected with prolonged treatment with these drugs raises the possibility of irreversible toxic effects on the brain, particularly the extrapyramidal system (Korczyn, 1972). There have been suggestions that the Parkinsonism effects, frequently observed with these drugs, might become irreversible after prolonged treatment (McGeer et al., 1961) or, conversely, disappear (Cahan andParish, 1960;Mandell and Oliver, 1961). The ideal way to answer this question-that is, to follow up patients maintained on the same dosage of neuroleptic drugs for several years-is not practical, and available information in the literature deals almost exclusively with the effects of relatively short periods of treatment. We have tried to approach the problem by measuring the extrapyramidal side-effects in patients treated with antipsychotic drugs for long periods, and correlating these manifestations with various parameters. In addition we have measured the protection offered by 1 Present address: Department of Physiology and Pharmacology, Sackler School of Medicine, Tel-Aviv University, Ramat-Aviv, Israel. (Accepted 21 April 1976.) orphenadrine against the extrapyramidal manifestations. It has been claimed that with prolonged treatment in Parkinson's disease orphenadrine loses efficacy (Strang, 1965), but there is no information concerning the effects of prolonged treatment in drug-induced Parkinsonism. METHODSThe population under study consisted of 66 psychiatric patients. These were among the 228 patients in seven long-stay wards at Goodmayes Hospital, Ilford, Essex. The rest of the patients in these wards had not been on major tranquillizers at the time of examination, or the dosage was not kept constant for any length of time before initiation of the study. The drugs used were chlorpromazine, thioridazine, trifluoperazine, fluphenazine, and haloperidol. The most common diagnosis was schizophrenia, either simple or paranoid.The patients were examined carefully neurologically, and special attention was given to the following signs and symptoms: hypokinesia, rigidity, trem...

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Section: Discussionmentioning

confidence: 98%

Extrapyramidal effects of neuroleptics.

Korczyn¹,

Goldberg²

1976

Journal of Neurology, Neurosurgery & Psychiatry

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“…This finding is consistent with the results of clinical reports and trials in Parkinson's disease patients, which also report no consistent improvement in motor tasks. Although the open-label studies generally demonstrated a positive effect of nicotine on motor symptoms (Marshall and Schnieden, 1966;Ishikawa and Miyatake, 1993;Kelton et al, 2000;Mitsuoka et al, 2002;Lemay et al, 2004;Hanagasi et al, 2007;Villafane et al, 2007), there was very little clinical efficacy of nicotine in the double-blinded trials, which also included significantly larger groups of patients (Fagerstrom et al, 1994;Clemens et al, 1995;Ebersbach et al, 1999;Vieregge et al, 2001;Shoulson, 2006). Although the variability of outcomes in the clinical studies may be due to differences in nicotine dosing, duration of treatment, outcome measure evaluated, small cohorts, and/ or clinical stage, the nature of the type of trial, that is, openlabel versus double-blinded, may be the important variable.…”

Section: Discussionmentioning

confidence: 99%

Nicotinic Receptor Agonists Reduce l-DOPA–Induced Dyskinesias in a Monkey Model of Parkinson's Disease

Zhang

Mallela

Sohn

et al. 2013

J Pharmacol Exp Ther

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Abnormal involuntary movements or dyskinesias are a serious complication of long-term L-DOPA treatment of Parkinson's disease, for which there are few treatment options. Accumulating preclinical data show that nicotine decreases L-DOPAinduced dyskinesias (LIDs), suggesting that it may be a useful antidyskinetic therapy for Parkinson's disease. Here, we investigated whether nicotinic acetylcholine receptor (nAChR) agonists reduced LIDs in nonhuman primates. We first tested the nonselective nAChR agonist 1, 6,7,8,9-tetrahydro-6,10-methano-6H-pyrazino [2,3-h][3]benzazepine (varenicline), which offers the advantage that it is approved by the U.S. Food and Drug Administration for use in humans. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned monkeys (n 5 23) were first administered L-DOPA/carbidopa (10/2.5 mg/kg) twice daily 5 days/week until stably dyskinetic. Oral varenicline (0.03-0.10 mg/kg) decreased LIDs ∼50% compared with vehicle-treated monkeys, whereas nicotine treatment (300 mg/ml in drinking water) reduced LIDs by 70% in a parallel group of animals. We next tested the selective a4b2*/a6b2* nAChR agonist heptane] on LIDs in the same set of monkeys after a 10-week washout. We also tested TC-8831 in another set of MPTP-lesioned monkeys (n 5 16) that were nAChR drug-naïve. Oral TC-8831 (0.03-0.3 mg/kg) reduced LIDs in both sets by 30-50%. After a washout period, repeat TC-8831 dosing led to a greater decline in LIDs (60%) in both sets of monkeys that was similar to the effect of nicotine. Tolerance to any nAChR drug did not develop over the course of the study (3-4 months). NAChR drug treatment did not worsen parkinsonism or cognitive ability. These data suggest that nAChR agonists may be useful for the management of dyskinesias in L-DOPA-treated Parkinson's disease patients.

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“…Na literatura, sobre a relação existente entre uso de nicotina e tremores em geral, existem estudos 11,12 que apontam para melhora imediata do tremor parkinsoniano, enquanto a nicotina pioraria outros tipos de tremores como o fisiológi-co, o induzido ou o tremor essencial. Porém, em um estudo de coorte prospectivo 11 , no qual foi observada a incidência de novos casos de tremor essencial entre fumantes e não fumantes, houve associação entre os casos de fumantes "pesados" na linha de base e baixo risco de desenvolvimento da doença.…”

Section: Relato De Casounclassified

Cessação tabágica em paciente com tremor essencial

Costa

Cotrik

Araújo³

et al. 2013

J. bras. psiquiatr.

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resUMoExistem pacientes que, apesar dos esforços da equipe do programa de cessação tabágica, mostram-se refratários à redução do tabagismo. Entre os motivos mais citados para isso, estão abuso de álcool, ansiedade e depressão. Além desses, o tremor essencial, frequentemente negligenciado pelos pacientes e médicos, tem implicações clínicas diretas e indiretas para aqueles que desejam parar de fumar. Antes entendida como uma doença benigna, o tremor essencial tem fortes associações com transtornos psiquiátricos, além de piorar com a abstinência de nicotina e com o uso de determinados medicamentos para a cessação. Descrevemos um caso de tremor essencial e comorbidades psiquiátricas no seu percurso para a abstinência tabágica. Com relação à associação entre nicotina e o curso do tremor essencial, maiores estudos são necessários. Mas diagnosticar sua presença apresenta relevância clínica, podendo ser um marcador de pior prognóstico para a cessação. aBstractThere are patients that are resistant to reducing tobacco use, despite the effort of the professionals helping them to quit. Among the most cited motives, there are alcohol abuse, anxiety and depression. Furthermore, frequently neglected by patients and doctors, essential tremor has direct and indirect clinical implications for those who want to stop smoking. Once known as a benign condition, essential tremor has strong association with psychiatric disorders and can get worse because of nicotine abstinence and certain medications used in smoking cessation. We report a case of essential tremor and psychiatric comorbidities on the path towards tobacco abstinence. Regarding the link between nicotine and the course of essential tremor, further studies are necessary. However, diagnosing its presence is clinically relevant and should be considered a marker of worse prognosis in smoking cessation.

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Effect of adrenaline, noradrenaline, atropine, and nicotine on some types of human tremor.

Cited by 75 publications

References 6 publications

Extrapyramidal effects of neuroleptics.

Extrapyramidal effects of neuroleptics.

Nicotinic Receptor Agonists Reduce l-DOPA–Induced Dyskinesias in a Monkey Model of Parkinson's Disease

Cessação tabágica em paciente com tremor essencial

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