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)

Tardive dyskinesia can be suppressed by drugs that block dopaminergic receptors, but often at the cost of a concomitant increase in parkinsonism. Sulpiride (400 -- 2100 mg/day), a selective type-2 dopamine receptor antagonist, was evaluated in a blind, placebo-controlled trial in 11 patients with tardive dyskinesia. It significantly (P less than 0.01) reduced tardive dyskinesia without significantly affecting parkinsonism, although three patients had a increase in preexisting parkinsonian hypokinesia and tremor. During the placebo phase, the tardive dyskinesia and parkinsonian scores returned to the pretreatment values. There was no relationship between either tardive dyskinesia or parkinsonism and eye blinking rates. These results are consistent with the hypothesis that more than one population of dopamine receptors are involved in controlling extrapyramidal function. Sulpiride is an important tool for elucidating both the practical and heuristic aspects of subtypes of dopamine receptors and is a lead in the search for compounds that selectively affect dopaminergic mechanisms.
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PMID:Sulpiride in tardive dyskinesia. 4 75

1. Twelve healthy male volunteers participated in four experimental occasions during each of which they were dosed with one of the following anti-psychotic drugs: chlorpromazine (50 mg), haloperidol (3 mg), sulpiride (400 mg) and placebo. Drugs were allocated to subjects in a double-blind, crossover fashion. 2. The subject's mood state, psychometric performance and electroencephalogram (EEG) were assessed pre-dose, and at 2, 4, 6, 8, 24 and 48 h post-dose. Mood states were assessed using 16 visual analogue scales and psychomotor performance was measured using the following tests: elapsed time estimation, tapping rate, choice reaction times, a rapid information processing task, flash fusion threshold, a manipulative motor task, digit span, body sway and tremor. 3. Chlorpromazine and haloperidol significantly reduced subjective ratings of 'alertness' and 'contentedness', and haloperidol significantly reduced feelings of 'calmness'. Sulpiride did not significantly affect any of the visual analogue scales. 4. All three anti-psychotic drugs had similar EEG effects with peak effect 2 to 4 h postdose. The profile was characterised by an increase in the proportion of slow wave activity (delta and theta) as well as decreased alpha (8-14 Hz) and faster (beta) wave activity. 5. Chlorpromazine reduced tapping rate and increased choice reaction movement times. Haloperidol reduced the flash fusion threshold frequency at 6 h post-dose. Sulpiride prolonged the duration of the manipulative motor task, particularly at 48 h post-dose. 6. All three anti-psychotic drugs impaired performance on the rapid information processing task. Chlorpromazine significantly reduced the number of correct letter pair identifications at 2, 4 and 6 h post-dose, haloperidol at 4, 6, 8, 24 and 48 h post-dose, and sulpiride at 24 h post-dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of the central nervous system effects of haloperidol, chlorpromazine and sulpiride in normal volunteers. 228 26

(+/-)Isofloxythepin (0.32-3.2 mg/kg, i.p.) significantly inhibited in a dose-dependent manner wet-dog shaking (WDS) induced by electrical stimulation of the rat hippocampus. In addition, both optical isomers of isofloxythepin inhibited WDS, with the (-)-isomer being almost 3 times more potent than the (+)-isomer. Other neuroleptics such as haloperidol, chlorpromazine, zotepine and sulpiride also reduced significantly the number of WDS. The inhibitory potency of haloperidol was comparable to that of (+/-)isofloxythepin, which was approximately 3 times more potent than that of chlorpromazine or zotepine. Sulpiride suppressed significantly WDS only at the high dose of 100 mg/kg. None of the drugs affected hippocampal afterdischarge. Inhibition of WDS produced by (+/-) isofloxythepin or haloperidol was antagonized by pretreatment with a dopamine receptor agonist, lisuride. The present results indicate that isofloxythepin shares with other neuroleptics an inhibitory effect on WDS; dopaminergic blocking action appears to be important in the inhibition of WDS induced by hippocampal stimulation.
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PMID:Effect of isofloxythepin, a novel neuroleptic, on hippocampal stimulation-induced wet-dog shaking in the rat. 256 2

Cocaine (5-40 mg/kg, intraperitoneally) enhanced locomotion and rearing accompanied with head circling and body shaking. Although at 40 mg/kg typical stereotypy licking occasionally appeared, 40% of the rats died. At doses that did not affect physiologic locomotion and rearing, the D1-receptor antagonist SCH23390 but not D2 antagonist raclopride inhibited locomotion and rearing stimulated by cocaine (20 mg/kg). All behavioral responses of cocaine were abolished with increasing doses of raclopride and SCH23390. Sulpiride, a D2 antagonist, exerted a biphasic effect on locomotor activity (i.e., a low dose of sulpiride increased and a high dose decreased cocaine-induced locomotor activity). Sulpiride enhanced head circling, body shaking, and increases of rearing induced by cocaine. D2-receptor agonists quinpirole and bromocriptine inhibited these responses, presumably by activating the typical stereotyped behaviors such as sniffing at low doses, and licking and gnawing at high doses. The lowest dose of bromocriptine inhibited all behaviors induced by cocaine without producing typical stereotyped behaviors in itself. SK+F38393, a D1-receptor agonist, in combination with cocaine did not induce typical stereotype, which results in a synergistic effect of D1 and D2-receptor activities. The increases of locomotion and rearing, head circling, and body shaking induced by cocaine may involve the indirect activation of postsynaptic D1 and D2 receptors, presumably via dopamine release, resulting from inhibition of the presynaptic D2 receptors. These results also provide evidence that the indirect stimulation of postsynaptic D2 receptors by cocaine (20 mg/kg) is insufficient to induce stereotyped behaviors, and that the role of dopamine D1 receptors in mediating the behavioral actions of acute cocaine appears to be more important than that of D2 receptors. Our results also suggest that bromocriptine may be useful for the treatment of acute cocaine poisoning.
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PMID:Involvement of D1 and D2 dopamine systems in the behavioral effects of cocaine in rats. 858 13

The present study analyzed the effect of intra-accumbens administration of the stereoisomers of sulpiride upon (3,4-dihydroxyphenylimino)-2-imidazoline (DPI)-induced changes in oral behaviours and electromyographic patterns of jaw muscles. In line with earlier findings, DPI (5 micrograms) administered into the nucleus accumbens increased chewing and tremor. l-Sulpiride (2-50 ng) had no effect on DPI-induced oro-facial behaviours. d-Sulpiride (10-50 ng) significantly antagonized the DPI-induced increase in chewing and had a biphasic effect on tremor with potentiation (10 ng) followed by attenuation (50 ng). When administered alone, l- or d-sulpiride did not affect oro-facial behaviours. The electromyographic signals, which were analyzed according to a previously described method, were described with the help of three classes: A (the seconds marked by frequency 3 Hz), B (the seconds marked by the frequencies 4-6 Hz); C (the seconds marked by the frequencies 7-15 Hz). DPI enhanced Class B and C of the masseter muscle but did not significantly affect any frequency class of the digastric muscle. l-Sulpiride (2-50 ng) had no effect on DPI-induced (5 micrograms) changes in electromyographic signals. d-Sulpiride (50 ng) antagonized the effects of DPI on Class B of the masseter muscle. Furthermore, d-sulpiride had a biphasic effect on Class C with potentiation (10 ng) followed by attenuation (50 ng). When administered alone, l- or d-sulpiride did not affect the frequency classes of the jaw muscles. It is concluded that d-sulpiride inhibits DPI-induced changes in oral behaviour and electromyographic patterns. It is suggested that d-sulpiride may be effective in the pharmacotherapy of oro-facial dyskinesias in man.
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PMID:d-Sulpiride inhibits oral behaviour elicited from the nucleus accumbens of freely moving rats. 884 11

Levosulpiride is a substituted benzamide that is widely used for the management of dyspepsia and emesis. However, little is known about levosulpiride-induced movement disorders (LIM). The aim of this study was to investigate the clinical characteristics of patients with LIM. Among 132 consecutive patients who were diagnosed with drug-induced movement disorders between January 2002 and March 2008, 91 patients with LIM were identified and their medical records reviewed. Seventy-eight (85.7%) patients were aged more than 60 years. The most common LIM was parkinsonism (LIP) (n = 85, 93.4%), followed by tardive dyskinesia (n = 9, 9.9%) and isolated tremor (n = 3, 3.3%). Twenty-one (24.7%) of the 85 patients with LIP were rated as Hoehn and Yahr stage III-V. The oro-lingual area was the only body part that was involved by tardive dyskinesia. LIM persisted after withdrawal of levosulpiride in 48.1% of patients with LIP, 66.7% with dyskinesia, and none with isolated tremor. None of clinical and MRI features predicted the reversibility of LIP. Levosulpiride frequently causes drug-induced movement disorders, presenting mainly with LIP followed by lower face dyskinesia. The symptoms are often severe, and irreversible even after the withdrawal of levosulpiride. Physicians should be cautious in using levosulpiride, especially in elderly patients.
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PMID:Levosulpiride-induced movement disorders. 1979 76

Levosulpiride is a newer prokinetic agent with increasingly extensive use in India by general physicians. Levosulpiride selectively inhibits gut and central D2 receptors and is associated with various movement disorders like- tremor, Parkinsonism, dyskinesias and rarely dystonia. We report 7 cases of levosulpirideinduced dystonia at our institute. Though all patient had at least 50% improvement after discontinuation of levosulpiride, none had complete recovery at mean follow up of 5.5 months. Through this article we want to highlight extrapyramidal side effects of levosulpiride, need of its awareness among physicians.
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PMID:Levosulpiride-Induced Dystonia: 7 Cases. 3133 Nov 48