Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metoclopramide hydrochloride is now commonly prescribed for a variety of gastrointestinal disorders. Over a 2-year period 18 patients with neurologic disorders induced by metoclopramide were assessed at the Parkinson's disease clinic of the Ottawa Civic Hospital. During metoclopramide therapy acute transient dystonic reactions were seen in 4 patients, and parkinsonism, which was frequently misdiagnosed and treated as classic Parkinson's disease, was seen in 12 patients. After treatment with metoclopramide was stopped, tardive dyskinesia appeared in seven patients and has persisted for up to 15 months in three patients. Parkinsonism and tardive dyskinesia occurred in older patients undergoing long-term therapy with metoclopramide. This experience, therefore, suggests that such treatment, especially in older patients, should be avoided.
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PMID:Adverse neurologic effects of metoclopramide. 705 69

Pergolide mesylate is a potent dopamine agonist that is being evaluated clinically in Parkinson disease, hyperprolactinemia, and other diseases. Pergolide activates both presynaptic and postsynaptic dopamine receptors, with some apparent selectivity for the presynaptic dopamine autoreceptors. In rats, low doses of pergolide (0.01 mg/kg or less, intraperitoneally) decreased dopamine turnover in brain, decreased serum prolactin concentration, and reduced blood pressure in spontaneously hypertensive rats. At somewhat higher doses (0.05 mg/kg or more, intraperitoneally), pergolide caused contralateral turning in nigrostriatal-lesioned rats, elevation of serum corticosterone, and hypermotility with stereotyped behavior. All of these actions are thought to be due to stimulation of dopamine receptors at various sites, but the data suggest that pergolide may have preferential affinity for presynaptic dopamine receptors. If low doses of pergolide can reduce dopaminergic transmission by activating presynaptic receptors that control dopamine release, then this action might be therapeutically useful in treating schizophrenia without causing tardive dyskinesia or in the treatment of tardive dyskinesia. The long duration of action of pergolide seen in animal and human studies could be an important advantage over some other dopamine agonists such as apomorphine.
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PMID:Degree of selectivity of pergolide as an agonist at presynaptic versus postsynaptic dopamine receptors: implications for prevention or treatment of tardive dyskinesia. 717 59

Dopamine (DA) is an important neurotransmitter or neuromodulator in the mammalian nervous system. As such, it is implicated in the aetiology and therapy of various disease conditions--for example, Parkinson's disease, schizophrenia, Huntington's disease and tardive dyskinesia. However, only limited electrophysiological information is presently available concerning dopamine receptors in the mammalian nervous system, and there are only three reports in which intracellular techniques have successfully recorded the action of DA on individual central neurones. In all cases, DA depolarised the respective neurones. In the periphery, DA is reported to hyperpolarise superior cervical ganglia. However, this hyperpolarisation has been shown to be due to activation of alpha-adrenoreceptors and not to a response of DA on a DA receptor. Peripheral DA actions have also been described presynaptically, but are difficult to study electrophysiologically for technical reasons. As a result, little is known at the membrane level about the effects of drugs thought to modulate or interact with DA receptors. In the present report, we describe a depolarising action for DA on the cat dorsal root ganglion.
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PMID:Dopamine depolarisation of mammalian primary afferent neurones. 735 66

Free radicals are highly reactive chemical species with an unpaired electron, and their formation is catalyzed by transition metals like iron, copper, and manganese. There have been numerous studies linking free radical damage with neuropsychiatric illnesses, including several psychiatric and motor disorders, raising the possibility that antioxidant strategies might serve a neuroprotective role for some conditions. The illnesses studied include tardive dyskinesia, schizophrenia, Parkinson's disease, and Alzheimer's disease. Although oxidative mechanisms may play a role in these conditions, further studies are necessary to define their involvement, and to determine the extent to which antioxidants may partially alleviate or prevent some of these conditions.
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PMID:Free radical involvement in neuropsychiatric illnesses. 767 80

Recent research on the role of clozapine in the treatment of Parkinson's disease and other movement disorders is discussed. Most clinical trials have shown resolution of or improvement in psychotic symptoms accompanying Parkinson's disease without worsening of parkinsonian symptoms. Adverse effects appear to be mild at dosages of < 100 mg/day; sedation is the most frequent problem. Most of these studies have serious limitations, however; until better studies have been completed, the decision to use clozapine for Parkinson's disease-related psychosis should be made on a case-by-case basis, with thorough evaluation of risks, benefits, and other therapeutic options. Some patients with Parkinson's disease have shown improvement in tremor and other abnormal movements when given clozapine. Clozapine cannot be recommended for treating tardive dyskinesia on the basis of the research done so far; some trials show dramatic resolution of symptoms, others no benefit. Anticholinergics or dopamine-reuptake inhibitors should be considered before clozapine is given to patients with tardive dyskinesia because of clozapine's potential for serious adverse effects. A few patients with Huntington's disease have responded to clozapine, but again no conclusions can be drawn. Clozapine appears to offer no real advantage over haloperidol for treating choreiform movements in Huntington's disease. The frequency of tics in Tourette's syndrome does not seem to be reduced by clozapine. Clozapine has shown some efficacy as a treatment for psychosis and abnormal movements in Parkinson's disease. Results have been less promising for other movement disorders. Further study in larger populations is needed before any definitive conclusions about clozapine's place in movement disorder therapy can be made.
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PMID:Clozapine therapy for Parkinson's disease and other movement disorders. 853 51

Iron is highly concentrated in the basal ganglia of the brain. The involvement of cerebral iron and its handling systems in neurodegenerative brain diseases like Parkinson's disease and tardive dyskinesia is currently under close investigation. There is evidence from animal studies that neuroleptics can increase iron uptake into brain. This effect appeared to be due to alteration of blood-brain barrier transport by the neuroleptics, particularly chlorpromazine and haloperidol, but not clozapine. We have investigated one Rhesus monkey using positron emission tomography (PET) and [Fe-52]-citrate before and during haloperidol administration. After drug withdrawal during a period of 1.5 year the investigation procedure was repeated. The results show that in the investigated monkey haloperidol induces a reversible marked increase of iron transport across the blood brain barrier concomitant with a large increase in elimination rate of the tracer from the blood.
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PMID:Blood to brain iron uptake in one rhesus monkey using [Fe-52]-citrate and positron emission tomography (PET): influence of haloperidol. 788 94

In the first section of this paper several aspects of tardive dyskinesia (TD) (clinical, epidemiological, pharmacological) are reviewed. We propose that this syndrome is not the consequence of dopamine receptor proliferation, but results from damage or degeneration of striatal cholinergic interneurons. We suggest that this cellular damage is caused by prolonged overactivation of these neurons, which occurs when they are released from dopaminergic inhibition following neuroleptic administration. Overactivity of central cholinergic systems during akinetic and motor retarded depression could be a contributory cause. The predisposition to L-DOPA-induced peak-dose dyskinesia in Parkinson's disease may depend on the same type of striatal neuronal loss. In the second part of the paper, the subject of supersensitivity psychosis and drug-resistant schizophrenia is reviewed. These two syndromes, are commonly associated with TD, have similar predisposing factors and pharmacology to TD, and are potentially persistent. We suggest that these conditions also result from degeneration of cholinergic striatal interneurons following chronic neuroleptic administration. The efficacy of clozapine for such treatment-refractory psychoses is explained in terms of its blockade of D-1 dopamine receptors. Other drugs effective against refractory psychoses (e.g. risperidone) are predicted to reduce activation at D-1 receptors.
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PMID:Loss of striatal cholinergic neurons as a basis for tardive and L-dopa-induced dyskinesias, neuroleptic-induced supersensitivity psychosis and refractory schizophrenia. 790 33

In this article the effect of vitamin E on two extrapyramidal disorders, tardive dyskinesia and Parkinson's disease, is reviewed. After a brief description of the symptoms, the current hypotheses for the pathogenesis of these diseases are described. A summary of the clinical research that has been done to establish the effectiveness of vitamin E is given. In tardive dyskinesia four clinical trials (double-blind, placebo-controlled) showed improvement in the symptoms with vitamin E in doses of up to 1,600 IU/day. Preliminary studies concerning Parkinson's disease suggested that vitamin E (2,000 IU/day) probably cannot prevent the development of the disease. It was suggested that vitamin E is able to slow the progression of the illness. The results from a large double-blind, placebo-controlled clinical trial, however, did not show any beneficial effect of vitamin E in Parkinson's disease.
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PMID:Vitamin E in extrapyramidal disorders. 822 Feb 97

A retrospective analysis of 812 patients admitted to the Ross Tilley Burn Centre between 1984 and 1992 resulted in 37 cases of burn injuries which were directly related to premorbid disabilities. The majority of these burns (83.8 per cent) occurred in the patient's home, most commonly as scald injuries in the bath tub, the shower, or following hot water spills. Nineteen patients were male, 17 were female. The median age was 58 years. Six patients had spinal cord disorders: four had traumatic cord damage, two had spina bifida. Six patients had seizure disorders. Five of these patients had been taking anti-seizure medications, but all had subtherapeutic blood levels on admission to hospital. Two patients had diabetes mellitus with peripheral neuropathies. Thirteen patients had four miscellaneous neurological disorders, including: tardive dyskinesia (two), CVA (four), Parkinson's disease (two), Alzheimer's disease (two), cerebral palsy (one), multiple sclerosis (one) and blindness (one). Three patients had a diagnosis of syncope. Two patients had emphysema, and four were morbidly obese. The average length of stay (LOS) for the disabled patients was 27.6 days for a median burn size of 10 per cent body surface area (BSA), compared to an average LOS for the general population of 25.7 days for a larger median burn size of 21 per cent BSA. The mortality rate was also much higher in the disabled population (22.2 per cent vs. 6.0 per cent). Most of these burn injuries were preventable. A series of burn prevention guidelines is presented, in an attempt to reduce the incidence of these burn injuries in disabled patients.
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PMID:Burns in the disabled. 850 62

To determine the prevalence, clinical signs and course of drug-induced Parkinsonism (DIP) in a general neurology practice, as well as to study the changing pattern of drugs implicated. Retrospective study of DIP patients seen between January 1981 and December 1993. Of the 306 cases of parkinsonism seen, 56.8% were induced or aggravated by drugs. This side effects is more frequent in women and often occurs in old age. The drugs implicated most often were cinnarizine, sulpiride and flupentixol. Forty-two patients took 2 drugs simultaneously, whereas 6 took 3. The number of DIP seen increased after 1986 and then remained stable through 1993. Between 1981 and 1988, the drug most often implicated was cinnarizine, though its relative impact decreased in later years. The most frequently seen form of presentation was rigidakinetic syndrome. Neither drug nor age influenced clinical presentation. Parkinsonism disappeared completely within a mean of 5 months in 142 (82%) patients. Twenty-eight (16%) developed Parkinson's disease. Six of them were symptom-free for 12 to 72 months (mean 40 months), whereas 22 never experienced relief from parkinsonism. Sixteen suffered tardive dyskinesia, a complication that was not associated with the use of any particular drug. More than half of the cases of parkinsonism seen in a neurology practice are drug induced or aggravated, generally by psychotropic drugs. The frequency has held steady for the past 6 years. The drugs implicated change as knowledge of their inducement of parkinsonism becomes known. The clinical picture is usually reversible.
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PMID:[Drug-induced or aggravated parkinsonism: clinical signs and the changing pattern of implicated drugs]. 871 70


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