Drug-Induced Parkinsonism and Other Movement Disorders

Ross, Robert T.

doi:10.1017/s0317167100030389

Cited by 31 publications

(7 citation statements)

References 89 publications

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“…This paper reviews drug-induced parkinsonism in particular its clinical features, pathophysiology and underlying mechanisms. Other drug-induced related movement disorders (tardive dyskinesias, chorea, etc) have been recently reviewed (Ross, 1990) and are not discussed here. (Gibb and Lees, 1988…”

Section: Introductionmentioning

confidence: 99%

Drug‐induced parkinsonism: a review

Llau

Rascol

et al. 1994

Fundamemntal Clinical Pharma

101

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The main clinical features, pathophysiology and underlying mechanisms of drug-induced parkinsonism are reviewed. The clinical manifestations of drug-induced parkinsonism are often indistinguishable from idiopathic Parkinson's disease. However, some subtle differences may exist: for example drug-induced parkinsonism is often associated with tardive dyskinesias, bilateral symptoms and the absence of resting tremor, etc. Besides toxins (eg manganese, carbon monoxide or MPTP), many drugs are known to produce parkinsonism: dopamine blocking drugs (true neuroleptics used as antipsychotics: phenothiazines, butyrophenones, thioxanthenes but also sulpiride, "hidden" neuroleptics prescribed as anti-nausea or anti-vomiting drugs (such as metoclopramide and other benzamide derivatives), dopamine depleting drugs (reserpine, tetrabenazine), alpha-methyldopa, calcium channel blockers (flunarizine, cinnarizine, etc). The putative role of other drugs (eg fluoxetine, lithium, amiodarone) as well as the therapeutic management of this side effect are reviewed.

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Section: Introductionmentioning

confidence: 99%

Drug‐induced parkinsonism: a review

Llau

Rascol

et al. 1994

Fundamemntal Clinical Pharma

101

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“…Degeneration, blockade, 6-OHDA (6-hydroxydopamine) or MPTP (1-methyl-4-phenyl-l,2,3,6-tetrahydropyridine) lesion and monoamine-depletion of the nigrostriatal dopamine (DA) system induce catalepsy and reduce locomotion in man, primates, and rodents (see Ross, 1990;B6dard etal., 1992;Jolicoeur and Rivest, 1992). The main symptoms of catalepsy-postural immobility (akinesia) and muscular rigidity (rigor) Colpaert, 1987) as well as impaired locomotion-were abolished by dopamine receptor agonists (see Wachtel, 1991).…”

Section: Introductionmentioning

confidence: 99%

Glycine site antagonists abolish dopamine D 2 but not D 1 receptor mediated catalepsy in rats

Kretschmer

Winterscheid

Danysz

et al. 1994

J. Neural Transmission

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Catalepsy--a state of postural immobility (akinesia) with muscular rigidity (rigor)--and reduced locomotion in animals are behavioral deficits showing similarities with symptoms of Parkinson's disease (PD). The effects of the glycine site antagonists 7-chlorokynurenate and (R)-HA-966 on haloperidol-(D 2 antagonist) and SCH 23390- (D 1 antagonist) induced catalepsy and reduced locomotion are investigated in rats. Both antagonists dose-dependently counteract dopamine D 2 receptor mediated catalepsy but they have no influence on locomotion. Neither 7-chlorokynurenate nor (R)-HA-966 has any effect on dopamine D 1 receptor mediated catalepsy. This finding is surprising, since NMDA receptor antagonists counteract both, dopamine D 1 and D 2 receptor mediated catalepsy. D 1 and D 2 receptors are located on different populations of neurons. Thus, the present findings suggest that these different neuronal populations have different sensitivity for ligands binding at the glycine binding site of the NMDA receptor.

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“…Therefore, we have focused on the LCa/Mg group to investigate potential causes of catalepsy. The duration of catalepsy was previously shown to increase with the degeneration of the nigrostriatal DAergic neuron pathway [8,9]. Here, the cataleptic behavior observed in LCa/Mg mice was transiently inhibited in a dose-dependent fashion by the administration of the antiparkinsonian drugs bromocriptine, L-DOPA or amantadine.…”

Section: Discussionmentioning

confidence: 72%

Pharmacological evaluation of catalepsy in low calcium and/or magnesium deficient feeding mice

Nakagawasai¹,

Taniguchi²,

Tanno³

et al. 2012

Health

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Populations from the Kii peninsula of Japan and Guam present a high incidence of amyotrophic lateral sclerosis and parkinsonism-dementia complex. It is thought that the low levels of calcium (Ca) and magnesium (Mg) in the drinking water are involved in the pathogenesis of these diseases. The present study aimed to test the hypothesis that catalepsy, a behavioral immobility and one of the Parkinsonian symptoms, may result from functionally impaired dopaminergic neurons in low Ca and Mg (LCa/Mg) fed mice. A group of mice fed with an LCa/Mg diet for 6 weeks was compared to a control group on a standard diet. Cataleptic symptoms such as akinesia and rigidity were measured using the bar test.

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Drug-Induced Parkinsonism and Other Movement Disorders

Cited by 31 publications

References 89 publications

Drug‐induced parkinsonism: a review

Drug‐induced parkinsonism: a review

Glycine site antagonists abolish dopamine D 2 but not D 1 receptor mediated catalepsy in rats

Pharmacological evaluation of catalepsy in low calcium and/or magnesium deficient feeding mice

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