Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Perioral behaviors induced by neuroleptic drugs have been interpreted as an animal model of tardive dyskinesia. However, these behaviors have also been induced or enhanced by physostigmine, a cholinesterase inhibitor. The latter result is contradictory to the clinical effect of physostigmine in human tardive dyskinesia. In view of this contradiction and other considerations, perioral behaviors have also been interpreted as a model of acute dystonia. The present experiments replicated an earlier failure to observe spontaneous perioral behaviors after long-term neuroleptic treatment in rats as well as the paradoxical effect of physostigmine. The effect of physostigmine was also compared to phenylmethanesulfonyl fluoride and methanesulfonyl fluoride, irreversible CNS active cholinesterase inhibitors. There were significant differences between the effects of the various cholinesterase inhibitors and their interactions with perioral behaviors and neuroleptic treatment. It is concluded that the effects of cholinesterase inhibitors on perioral behaviors in rodents may not be accounted for entirely by cholinesterase inhibition. Further experiments using additional agonists and antagonists will be required to clarify the behavioral effects of these cholinesterase inhibitors.
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PMID:Perioral behaviors induced by cholinesterase inhibitors: a controversial animal model. 380 24

The effects of botulinum toxin-A was compared on both extrafusal and intrafusal muscle fibers in the biceps femoris of Wistar rats. Four days after injection no action potentials were elicited with stimulation single-fiber electromyography on the injected side. Fourteen days after injection, jitter became measurable and these values were increased on the injected side. Extrafusal muscle fibers began to atrophy on the 4th day and this continued to the 14th day postinjection. Atrophy was also evident and progressive in intrafusal muscle fibers. Increased terminal innervation ratios, end-plate spread of cholinesterase, and increased density of very small myelinated fibers in large intramuscular nerves were observed 14 days postinjection. Both extrafusal and intrafusal fibers are cholinergically innervated, and both were progressively affected by botulinum toxin, perhaps varying in degree only. In addition to partial denervation, Botulinum toxin effects in dystonia may also be related to modified spindle afferent discharge.
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PMID:Extrafusal and intrafusal muscle effects in experimental botulinum toxin-A injection. 862 28

A 14-year-old female attempted suicide by ingesting the organophosphate methyl parathion. A severe acute poisoning developed with the characteristic symptomatology: muscarinic, nicotinic and neurologic, as well serum cholinesterase activity decreased 88%. An extrapyramidal syndrome appeared suddenly nine days after the onset with ocular and buccal crisis, neck and trunk dystonic movements, and hypertonia and tremors. The patient improved with the administration of i.v. diphenhydramine. Other causes of toxic extrapyramidalism and organophosphate intermediate syndrome were discarded. Although an absolute causal relationship of the transient extrapyramidal symptomatology to the organophosphate exposure cannot be clearly established in this case, we speculate a possible delayed inhibition of the dopaminergic receptors in the substantia nigra and the basal ganglia.
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PMID:[Acute methyl parathion poisoning with extrapyramidal manifestations not previously reported]. 1020 15

Long-term administration of antipsychotics occasionally produces persistent dystonia of the trunk, a disorder known as Pisa syndrome (or pleurothotonus). The development of Pisa syndrome is most commonly associated with prolonged treatment with antipsychotics; however, it has also been reported, although less frequently, in patients who are receiving other medications (such as cholinesterase inhibitors and antiemetics), in those not receiving medication (idiopathic Pisa syndrome) and in those with neurodegenerative disorders. Drug-induced Pisa syndrome predominantly develops in females and in older patients with organic brain changes. It sometimes occurs after the addition of another antipsychotic to an established regimen of antipsychotics or insidiously arises in antipsychotic-treated patients for no apparent reason. The condition generally disappears after antipsychotic drugs are discontinued. Although a pharmacological therapy for drug-induced Pisa syndrome has not been established, we have reported that anticholinergic drugs are effective in about 40% of patients who have episodes of Pisa syndrome with the remaining patients responding to the withdrawal or reduction of daily doses of antipsychotic drugs. The characteristics of its development and prognosis indicate that drug-induced Pisa syndrome consists of two types of dystonia. Some patients develop clinical features of acute dystonia, whereas others develop symptoms similar to tardive dystonia. Like that of tardive dystonia, Pisa syndrome responds better than tardive dyskinesia to a relatively high daily dose of an anticholinergic. However, the significant improvement caused by the withdrawal of antipsychotic drugs in Pisa syndrome differentiates it from tardive dystonia. Thus, Pisa syndrome including these features is considered to be an atypical type of tardive dystonia. These clinical characteristics suggest that the underlying pathophysiology of drug-induced Pisa syndrome is complex. A dopaminergic-cholinergic imbalance, or serotonergic or noradrenergic dysfunction, may be implicated. Asymmetric brain functions or neural transmission may also be considered as underlying mechanisms of the development of Pisa syndrome that is resistant to anticholinergic drugs. Idiopathic Pisa syndrome is characterised by an adult-onset, segmental truncal dystonia in patients with no previous exposure to antipsychotics. It occurs rarely but shows a complete resolution with high doses of anticholinergic drugs.
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PMID:Drug-induced Pisa syndrome (pleurothotonus): epidemiology and management. 1188 37

Pisa syndrome is a rare type of truncal dystonia. Its development is associated commonly with neuroleptic treatment, but there are rare idiopathic cases or those related to neurodegenerative disorders. Recently, an association between cholinesterase inhibitors and Pisa syndrome has been described. The authors report two patients, one with Alzheimer's disease treated with risperidone and another with Parkinson's disease who presented this kind of dystonia after donepezil initiation. In the first patient the condition resolved after discontinuation of risperidone, and in the second one the condition resolved when donepezil was withdrawn. In patients with pharmacologic or degenerative dopaminergic neurotransmission disorders, cholinergic excess may induce this peculiar type of dystonia.
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PMID:Cholinergic-dopaminergic imbalance in Pisa syndrome. 1278 13

We describe 4 cases of delayed extrapyramidal disorder following acute dichlorvos poisonings. All patients were seriously poisoned since all exhibited profound coma and respiratory failure, and they were all tracheally intubated and mechanically ventilated. On admission, plasma cholinesterase activity was greaty decreased, < 10 micromol/ml/h at 37 C in all patients (< 10% of normal for our laboratory). Extrapyramidal symptoms occurred between 5 and 15 d and were characterized by dystonia of arms and legs, resting tremor, cogwheel rigidity, and hypereflexia. With bromocriptine therapy the features of extrapyramidal syndrome disappeared progressively with complete recovery in all patients. Our observations suggest a delayed extrapyramidal syndrome should be taken into account during the course of acute dichlorvos organophosphate poisonings.
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PMID:Extrapyramidal syndrome as a delayed and reversible complication of acute dichlorvos organophosphate poisoning. 1530 89

(1) Three cholinesterase inhibitors are marketed in France for the treatment of Alzheimer's disease: donepezil, galantamine and rivastigmine. Tremor and dystonia are known adverse effects of cholinesterase inhibitors. (2) In patients with Parkinson's disease who have cognitive disorders, or in patients with Lewy body dementia, exacerbations of parkinsonism and tremor have been observed during treatment with cholinesterase inhibitors at normal doses. The disorders were reversible on withdrawal of the cholinesterase inhibitor. (3) Withdrawal of cholinesterase inhibitors should be considered if gait disorders, falls or parkinsonism occur or worsen during treatment.
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PMID:Cholinesterase inhibitors: tremor and exacerbation of Parkinson's disease. 1792 35

We herein report an 81-year-old woman with Alzheimer's disease (AD) in who donepezil, a cholinesterase inhibitor (ChEI), caused cervical dystonia. The patient had a two-year history of progressive memory disturbance fulfilling the NINCDS-ADRDA criteria for probable AD. Mini-Mental State Examination score was 19/30. The remaining examination was normal. After a single administration of donepezil (5 mg/day) for 10 months, she complained of dropped head. Neurological examination and electrophysiological studies supported a diagnosis of cervical dystonia. Antecollis disappeared completely at 6 weeks after cessation of donepezil. Dystonic posture can occur at various timings of ChEI use. Physicians should pay more attention to rapidly progressive cervical dystonia in ChEI-treated AD patients.
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PMID:Donepezil-induced cervical dystonia in Alzheimer's disease: a case report and literature review of dystonia due to cholinesterase inhibitors. 2478 94