Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It was discovered by serendipity that a combined application of chlorpromazine (3.5 mg/kg) and pentobarbitone (20.0 mg/kg) induced intermittent tremor-bursts in four extremities of guinea pigs. This tremor with a prominent extensor activity disappeared after spinalization, indicating a supraspinal process. Biperiden reduced the frequency and amplitude of the tremor, which was further diminished by amantadine. Baclofen was found to be most potent drug in suppressing tremor. It was suggested that the cortico-striato-pallido-thalamo-cortical feedback loop may be impaired by a combined action of chlorpromazine and pentobarbitone. This new animal model for drug-induced tremor would be of considerable importance with regard to physiological, biochemical, pharmacological and pathological aspects of motor control.
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PMID:Intermittent tremor-bursts induced by chlorpromazine and pentobarbitone in guinea pigs: a new tremor model. 182 83

The effects of anticholinergic and dopaminergic drugs used for Parkinson's disease were studied on the tremor induced by physostigmine (0.3-3.0 mg/kg) in rats. For the measurement of tremor a new electronic device was employed. Atropine (0.3-1.2 mg/kg) and biperiden (0.01-1.0 mg/kg) reduced the physostigmine-induced tremor in a dose-related manner and could abolish it. Biperiden was less potent than atropine. Methylatropine in a dose of 1.2 mg/kg slightly inhibited the tremor. Amantadine (0.3-3.0 mg/kg) reduced the tremor but only to a certain degree. Bromocriptine (0.1-10.0 mg/kg) reduced it in a manner that was not dose-related. Pimozide potentiated the tremor in the dose of 0.2 mg/kg but not in larger doses. At the onset of the tremor, a small decrease in rectal temperature occurred. The hypothermia lasted significantly longer than the tremor. Neither the anticholinergic nor the dopaminergic anti-Parkinson drugs altered the hypothermic effect of physostigmine. The results show that those anti-Parkinson drugs, which act by increasing the dopaminergic activity can counteract the tremor induced by physostigmine. However, these drugs are clearly less active than th anticholinergic anti-Parkinson drugs.
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PMID:Drugs for Parkinson's disease reduce tremor induced by physostigmine. 662 15

The nature of the antagonism by anticholinergic compounds of nicotine-induced convulsion in mice has not been defined clearly. Although, because they do not compete effectively for agonist binding to brain tissue in-vitro, these compounds are thought to be non-competitive antagonists in the brain, pharmacological evidence is lacking. This study describes the anti-nicotinic properties of the clinically used anticholinergic antiparkinson drugs, benztropine, biperiden, caramiphen, ethopropazine, procyclidine and trihexyphenidyl. Nicotine-induced convulsion and arecoline-induced tremor in mice were effectively prevented by these drugs. The concentrations of benztropine, biperiden, caramiphen, ethopropazine, procyclidine and trihexyphenidyl affording 50% prevention of nicotine-induced convulsion (ED50 values) were 7.4, 4.6, 7.8, 4.9, 3.1 and 3.3 mg kg(-1), respectively. The classical muscarinic receptor antagonist atropine had potent anti-muscarinic effects but very weak anti-nicotinic activity. The classical nicotinic receptor antagonist mecamylamine had potent anti-nicotinic activity but no anti-muscarinic effects. The pattern of shift of the dose-response curve for nicotine-induced convulsion in mice was determined in the presence of increasing concentrations of the anticholinergic antiparkinson drugs. These drugs were found to increase the ED50 (0.49 mg kg(-1)) of nicotine-induced convulsion in a dose-related manner. The maximum effect of nicotine and the slope of nicotine dose-response curve were not significantly influenced by either low or high doses of benztropine, procyclidine or trihexylphenidyl, which suggests competitive action. Biperiden, caramiphen and ethopropazine, at low doses which significantly increased the ED50 of nicotine, did not affect the maximum effect of nicotine or the slope of the nicotine dose-response curve; at higher doses, however, they reduced the maximum effect and the slope, which suggests that these drugs have both competitive and non-competitive properties in antagonizing nicotine-induced convulsion in mice. The experiments demonstrate that the anticholinergic antiparkinson drugs and mecamylamine effectively antagonize nicotine-induced convulsion, but atropine does not; some of these drugs have competitive properties whereas others seem to have both competitive and non-competitive properties in antagonizing nicotine-induced convulsion in mice.
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PMID:Anti-nicotinic properties of anticholinergic antiparkinson drugs. 987 18

Tremorine-induced tremors model is used to evaluate antiparkinsonian drugs because rest tremor is a sign that distinguishes Parkinson's disease (PD) from other diseases. The effects of crude ethanolic extract (CEE) and total acetate fraction (TAF) of Plumbago scandens were investigated at several doses. These extracts at doses of 125 and 250 mg/kg i.p. failed to reduce tremors in tremorine-treated mice. TAF showed significant effects only at a dose of 500 mg/kg. Both CEE and TAF at doses of 1000 and 2000 mg/kg i.p. suppressed the tremors in a dose-dependent fashion for 60 min. Biperiden, an anticholinergic drug, was used as standard at a dose of 3 mg/kg i.p. This study suggests that P. scandens is a plant with possible therapeutic value for PD.
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PMID:Antiparkinsonian-like effects of Plumbago scandens on tremorine-induced tremors methodology. 1558 83

A 33 year-old male presented with right upper limb rest tremor that disappeared on action, posture associated with bradykinesia, and rigidity of right upper and lower limbs (Video S1). Patient also presented right-sided pyramidal weakness (grade 4), hyperreflexia, extensor plantar response, and hemihypesthesia. Skull X-ray and computed tomography (CT) of the brain showed several metal pellets producing multiple artifacts (Fig. 1A,B). Only one pellet settled in brain parenchyma (left midbrain), while other pellets settled in the skull bone (Fig. 1A). Transcranial sonography (TCS) was performed, confirming that the midbrain pellet was placed within the left substantia nigra (Fig. 1C). Levodopa challenge test was conducted, showing no improvement (pre- and post-l-dopa motor UPDRS were 21 and 20, respectively). A further chronic trial of l-dopa (for 3 months) also proved negative. Biperiden and propranolol were also tried with negative results. Figure 1Computed tomography (CT) of the brain and X-ray skull showed several pellets that produced multiple streak artifacts (Fig. 1A,B). Only one pellet rested in the brain parenchyma, the left (contralateral) midbrain as detected by CT (Fig. 1A), and transcranial sonography (Esaote MyLab Five, Providian, Italy) via temporal window (Fig. 1C). Abbreviations: SN, substantia nigra.Hemiparkinsonism has been previously reported secondary to midbrain lesions.1, 2 To the best of our knowledge, movement disorders (secondary to brain injuries) related to bullet fragments have been scantly reported. In one reported case, hemiparkinsonism and dystonia were the result of a bullet in midbrain,2 and in another, dystonia was caused by a bullet in internal capsule.3.
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PMID:Patient with Hemiparkinsonism Secondary to a Gun Pellet in the Contralateral Substantia Nigra. 3086