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)

The occurrence of acute dystonic reactions was studied relative to drug pharmacokinetic parameters following a single dose of the phenothiazine, butaperazine. Dystonias occurred more than one half-life from peak butaperazine levels, 23 to 56 h after drug administration. The authors postulate that the appearance of dystonias on falling plasma concentrations may be due to disruption of dopaminergic-cholinergic balance caused by differential antidopaminergic and anticholinergic potencies of the drug.
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PMID:Dystonic reactions following neuroleptics: time course and proposed mechanisms. 0 43

Pharmacokinetics of the phenothiazine, butaperazine, were studied in relationship to acute dystonic reactions. Dystonias appeared on falling drug concentrations, more than one half-life after plasma and red blood cell (RBC) peak butaperazine concentrations. Red blood cell butaperazine kinetics differentiated better than did plasma butaperazine levels those subjects in whom dystonias would develop from those in whom they did not. We conclude that RBC phenothiazine levels may more clearly reflect drug concentration at critical brain sites than do simple plasma drug levels. Furthermore, dystonic reactions may be the result of differential sensitivity of two or more receptor systems to receptor blockade by antischizophrenic agents.
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PMID:Pharmacokinetics of red blood cell phenothiazine and clinical effects. Acute dystonic reactions. 0 25

The changes occurring in hemodynamics due to the effect of alpha-adreno-blocking agent pyrroxan and beta-blocking agent obzidan were studied in 20 patients with neurocirculatory dystonia and in 20 patients with stage IIB hypertensive disease. Forty healthy persons formed the control group. The results of the investigation allow for the assumption that a pharmacological test with a record of the transthoracic rheogram and the derivatives of the central pulse tracings help in the proper choice of the drug and its dosage with the state of hemodynamics and the inotropic myocardial reaction taken into account.
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PMID:[Determination of the individual changes in cardiovascular system reactivity in prescribing adrenergic blockaders]. 2 49

Representative studies which elucidate present treatment principles regarding parenteral administration of neuroleptics for acute psychoses with agitation are reviewed. "Rapid tranquillization" with drugs such as haloperidol generally appears preferable, but controlled comparisons with more conservative types of treatment are lacking. It is suggested that parenteral chlorpromazine should be avoided because of its tendency to provoke severe hypotension, whereas loxapine apparently is a valuable drug if strong sedation is required for behavioural control. Possible advantages of ultra-high-dose therapy need to be proved in controlled trials, and the occurrence of toxic side-effects requires further evaluation. From an ethical and psychological point of view, it is recommended that antiparkinsonian medication should be administered simultaneously with neuroleptics which induce a high incidence of acute dystonia. Several types of acute psychosis with agitation which do not require treatment with a neuroleptic as drug treatment of first choice are briefly mentioned.
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PMID:Parenteral treatment of acute psychotic patients with agitation: a review. 3 May 96

The effectiveness of antiparkinson medication for the prevention of drug induced dystonias has remained a question. Forty patients with acute psychosis who received high potency oral antipsychotic drugs were interviewed to determine the incidence of acute dystonia. An eleven-fold increase in dystonia was found in patients who received no prophylactic medication. Such prophylaxis appears effective in preventing acute dystonia.
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PMID:Benztropine prophylaxis of dystonic reactions. 3 44

The authors studied the effects of tiapride in 28 patients with various painful conditions, tremors and abnormal movements, and behavioural disorders admitted to a Rehabilitation Centre. Good results were obtained in the painful conditions, especially following amputations, and in those with dystonia. Side-effects were very rarely observed, caused little disturbance to the patient, and were immediately reversible.
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PMID:[A study of a neurotropic product in a rehabilitation centre (author's transl)]. 3 42

The awareness of extrapyramidal reactions during initiation of neuroleptic treatment was studied in 14 patients. Only one patient spontaneously identified the presence of dystonia. The other 13, including 3 who had experienced extrapyramidal reactions during previous hospitalizations, did not fully identify the presence of symptoms, although several had vague discomfort. There was marked variability in acknowledgement of symptoms in response to prompting by staff members. The findings are similar to reports of agnosia for hemiparesis after parietal lobe injury and also to descriptions of agnosia in animals caused by destruction of dopaminergic neurons. Since extrapyramidal reactions represent blockade of dopaminergic neurotransmission, patients' inability to perceive the reactions may represent evidence for catecholaminergic modulation of sensory perception.
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PMID:Patients' awareness of extrapyramidal reactions to neuroleptic drugs: possible evidence for the role of catecholamines in perception. 4 27

Selected lysosomal hydrolases have been investigated in the trigeminal ganglion of mice afflicted with an hereditary sensory neuropathy (dystonia musculorum). This was done using direct enzyme histochemistry. Correlative electron microscopy was also used to further elucidate perikaryal changes. The earlies observed lesion in the trigeminal ganglion of afflicted mice was numerous axon swellings containing intense lysosomal hydrolase activity. Subsequent to this observation, numerous neurones showed central chromatolysis, eccentric nucleus and increased lysosomal hydrolase activity. As various neurones throughout the ganglion underwent the classical chromatolytic reaction, the Golgi apparatus moved to a juxtanuclear location, and there was a focal juxtanuclear accumulation of lysosomes. During the later stages of the disease, a striking decrease in neuronal hydrolase activity characteristic of neuronal atrophy was observed. These results are consistent with earlier suggestions that loss of sensation in the disease could be due to an interruption of axonal transport in primary sensory of neurones.
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PMID:Lysosomal hydrolases in the trigeminal ganglion of mice afflicted with an hereditary sensory neuropathy (dystonia musculorum). 5 73

In 4 out of 11 cebus apella monkeys given haloperidol (0.05 - 1.0 mg/kg/d) orally for up to 35 months signs of tardive dyskinesia (TD) hav developed: 1) One monkey developed barely noticeable TD after 4 months, but showed marked and increasing symtpoms of both generalized choreic and buccolingual TD after 8 months. This animal died 3 months after discontinuation of haloperidol. At that time the signs of TD were still prominent. 2) In one monkey bucco-lingual TD appeared after 3 months and was still reversible on discontinuation of haloperidol at 5 months. After a further 12 months of haloperidol, the TD signs proved to be long lasting, possibly irreversible, in this animal. 3) A third monkey showed slight and transient signs of TD at 14 months, but following a further 20 months af haloperidol administration a choreiform syndrome became porminent after drug withdrawal. 4) After 34 months a similar syndrome of choreic movements has been noticed in another animal, increasing after withdrawal of haloperidol. The other 7 monkeys have received haloperidol for 3 - 15 months, without developing any signs of TD. Attacks of acute dystonia have been noticed in all animals, sometimes necessitating anticholinergic medication or decreases in the daily haloperidol dose.
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PMID:Development of acute dystonia and tardive dyskinesia in cebus monkeys. 11 74

Cebus apella monkeys subjected to chronic haloperidol administration develop neurologic disturbances very similar to neuroleptic-induced acute dystonia human beings. After varying lengths of time, certain monkeys develop a prolonged dyskinetic syndrome resembling tardive dyskinesia (TD), as seen clinically. Two monkeys with signs of TD were given single intramuscular injections of various compounds with known effects on the catecholaminergic, cholinergic, serotoninergic and GABA-ergic neurotransmittor systems, and their effect on the TD signs were rated. Dopamine receptor blockers as well as cholinergics had an ameliorating effect on the symptoms. Some compounds known to activate the GABA system, including some benzodiazepines and the GABA-transaminase inhibitor amino-oxyacetic acid, also reduced the symptoms, as did the serotonin precursor L-5HTP. Results with serotonin antagonists were equivocal. It is concluded that dopamine receptor blockade, as well as increased activity within the GABA-ergic or cholinergic systems cause alleviation of TD. The findings are in agreement with earlier reports in man and thus seem to validate this primate model.
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PMID:Pharmacological modification of experimental tardive dyskinesia. 11 27


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