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)

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 paper deals with a study of the nervous system in 121 patients with acute poisening with dichlorethane. Among the studied contingent there were 110 males and 11 females. According to the severity of the intoxication the patients were divided into 3 groups: mild--23 cases, moderate--11 cases, severe--87 cases. The following 6 neurological syndromes were distinguished: comatose, convulsive, atactic, extrapyramidal, psychotic and asthenic with vegetative-vascular insufficiency. Morphological studies detected the following: congestion plethora, vascular dystonia, microfoci hemorrhages, acute swelling of the nervous cells with signs of chromatolyses, shrunk cells, severe and ischemic change of the nervous cells. The treatment consisted in an accelerated elimination of dichlorethane from the organism and symptomatic therapy. The results of these studies demonstrated that in poisoning with dichlorethane there were diffuse, mainly dystrophic changes in the cells of the brain and spinal cord, which clinically may be expressed by symptoms of a lesion of many systems and may be qualified as toxic encephalomyelopathy.
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PMID:[Neurologic disorders in acute dichloroethane poisoning]. 66 65

The dopaminergic neurons of the substantia nigra pars compacta and ventral tegmental area play a crucial role in regulating movement and cognition respectively. Several lines of evidence suggest that a degeneration of dopaminergic cells in the substantia nigra produces the symptoms of Parkinson's disease. On the other hand, a hyperactivity of the dopaminergic transmission in the brain induces dyskinesia, dystonia and psychosis. It is also well established that the euphoric and rewarding responses evoked by drugs of addiction, such as amphetamine and cocaine, are mediated by central dopamine systems. Electrophysiological experiments which study the activity of single dopaminergic neurons in the ventral mesencephalon have shown that dopamine and dopaminergic drugs reduce the firing frequency of these cells. This is due to the stimulation of D2-D3 autoreceptors and to a hyperpolarization of the membrane produced by an increase in potassium conductance. In addition, substances which increase the release (amphetamine), the synthesis (levodopa) or block the uptake (cocaine, nomifensine, amineptine) of dopamine in the brain inhibit the firing activity of the dopaminergic cells throughout dopamine-mediated mechanisms. In this review, we will briefly examine the literature concerning the physiological and behavioural responses caused by dopamine and dopaminergic agents on the dopaminergic neurons of the ventral mesencephalon. Our conclusion suggests that the electrophysiological actions of dopamine and dopamine-related drugs on dopaminergic cells in the ventral mesencephalon might be indicative of the pharmacological effects of these agents on the brain.
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PMID:The electrophysiological actions of dopamine and dopaminergic drugs on neurons of the substantia nigra pars compacta and ventral tegmental area. 135 54

We analyzed 71 patients (45 males and 26 females) with Wilson's disease (WD) who were seen at our hospital from 1979 through 1990. The mean age at onset was 18.1 +/- 6.5 years, with 17.0 +/- 6.6 years for males and 20.2 +/- 5.7 years for females. The mean age at the time of diagnosis was 21.0 +/- 6.3 years. Hepatic WD was the most frequent mode of presentation in childhood with a mean age of 15.5 +/- 6.0 years, while neurologic WD tended to occur in adolescence with a mean age of 21.0 +/- 8.9 years. The ages of onset were 12.5 +/- 0.5 years for renal WD and 25.3 +/- 2.4 years for psychiatric WD. The common initial symptoms were neurologic and hepatobiliary. In addition, hematologic and renal disorders were also common during evaluation. The neurologic findings at the time of diagnosis were tremors (66.2%), dysarthria (56.3%), gait disturbances (46.5%), dystonia (42.3%) and decreased facial expressions (40.8%). Less frequent but notable neurologic presentations were psychosis (11.3%), epileptic seizures (5.6%) and hypokalemic periodic paralysis (1.4%). When compared with two previous large Chinese series, the present data show a male preponderance, an earlier age of onset for males and higher incidences of hepatic, hematologic and renal involvement. The possible reasons for the discrepancies between the present study and previous Chinese series are discussed.
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PMID:Wilson's disease: clinical analysis of 71 cases and comparison with previous Chinese series. 135 28

This report describes a patient with schizophrenia who developed episodes of ocular dystonia as a delayed side effect of neuroleptic medication. Each episode was preceded and accompanied by marked agitation, stereotypic behaviour and exacerbation of hallucinations. Both the psychotic and dystonic symptoms responded to anticholinergic medication. The theoretical and practical implications of this observation are discussed.
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PMID:Psychotic symptoms preceding ocular deviation in a patient with tardive oculogyric crises. 136 53

Veralipride is a benzamide derivative effective in the treatment of menopausal syndrome. Despite its antidopaminergic action, extrapyramidal side effects seem to be very uncommon. We observed a patient with bipolar psychosis, who developed segmental dystonia after taking the drug. The disorder slowly receded in 14 months, but reappeared during neuroleptic therapy a few months later. To the best of our knowledge, this is the first case of veralipride-induced tardive dystonia, and the affective disorder might have predisposed our patient to the development of this tardive side effect.
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PMID:Veralipride-induced tardive dystonia in a patient with bipolar psychosis. 142 99

The authors describe the clinical phenotypes of hexosaminidase deficiencies (GM2 gangliosidosis). The symptoms, differently combined, include cerebellar ataxia, motor neuron disease, dystonia, psychosis, neurovegetative troubles with different severity. Morphological changes are evident in rectal, muscle or nerve biopsies. Minor clinical changes are described in carriers from a family. A chronic GM2 gangliosidosis has to be suspected in any atypical case with the above-mentioned symptoms with autosomal-recessive inheritance.
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PMID:The clinical aspects of adult hexosaminidase deficiencies. 184 98

Of 125 patients with neuroleptic (dopamine blocking) drug-induced movement disorders who had been referred to a specialized clinic to differentiate the predominant movement disorder, 63% had tardive dyskinesia, 30% had parkinsonism, 24% had dystonia, 7% had akathisia, and 2% had isolated tremor. Two or more movement disorders coexisted in 31 patients (25%). Functional disability was more severe in patients with akathisia than in other patients. Women outnumbered men at a ratio of 4:1, except for tardive dystonia which affected both sexes equally. The average at onset was 56 years (range, 13 to 87); 69 patients (55%) had onset of movement disorder in the sixth decade. While tardive dystonia was distributed relatively evenly in all age groups, almost a third of patients with parkinsonism had it in the eighth decade. Haloperidol was implicated in 47 patients (37%), followed by amitriptyline/perphenazine in 30%, thioridazine in 27%, and chlorpromazine in 20%. Metoclopramide-induced movement disorders were found in 10 (8%). Most patients (101 or 81%) had history of psychiatric illnesses, but of these only 44 had psychosis. Neuroleptic drugs had been prescribed for 33 patients (26%) who had gastrointestinal problems. It is important to recognize and differentiate various drug-induced movement disorders because such differentiation has pathophysiologic and therapeutic implications. Many patients could have been treated with less potent drugs.
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PMID:Neurologic approach to drug-induced movement disorders: a study of 125 patients. 197 59

1. Neuroleptic drugs (antipsychotics) produce numerous side effects which include serious extrapyramidal symptoms consisting of akathisia, dystonia, neuroleptic malignant syndrome, parkinsonian reactions such as postural abnormality, tremor, akinesia or bradykinesia, rigidity, and tardive dyskinesia. 2. Among the complications of neuroleptic chemotherapy, the most serious and potentially fatal complication is malignant syndrome, which is characterized by extreme hyperthermia, "lead pipe" skeletal muscle rigidity causing dyspnea, dysphagia, and rhabdomyolysis, autonomic instability, fluctuating consciousness, leukocytosis, and elevated creatine phosphokinase. 3. Neuroleptic malignant syndrome should be differentiated from malignant hyperthermia, lethal catatonia, and other pathological states producing some of these same symptoms. 4. In addition to neuroleptics, malignant syndrome has been caused by thymoleptics (antidepressants), metoclopramide (antiemetic), metoclopramide combined with cimetidine, tetrabenazine, overdosage of benzodiazepine, phenelzine, dothiepin and alcohol, and amphetamine. 5. Factors leading to and/or facilitating the emergence of neuroleptic malignant syndromes are reportedly organic brain syndrome, dehydration, exhaustion, external heat load, excessive sympathetic discharge, use of long acting neuroleptics, high doses of neuroleptics, rapid dose titration with neuroleptics, abrupt discontinuation of antiparkinsonism agents, and concurrent lithium therapy. 6. Although, the pathogenesis of neuroleptic malignant syndrome is not understood completely, a blockade of dopaminergic receptors in the hypothalamus, spinal cord and striatum, an alteration of dopaminergic-serotonergic transmission in the body, an enhanced synthesis and action of prostaglandin E1 and E2, and a modification of calcium-mediated signal transduction in the body have been suggested. 7. The treatment of malignant syndrome includes immediate withdrawal of neuroleptic drugs, i.v. infusion of dantrolene, and oral administration of bromocriptine; or alternatively i.v. infusion of dantrolene and the combination of levodopa-carbidopa. 8. Other measures to enhance the therapeutic effectiveness of the aforementioned regimens are to include the use of anticholinergic drugs such as benztropine to enhance the effectiveness of bromocriptine, of lorazepam if catatonic symptoms persist, or of electroconvulsive therapy (ECT) if psychotic symptoms persist. 9. These treatments, however, must be "active" rather than "passive", in order to avert fatalities and/or unfortunate sequelae from this iatrogenic and incompletely understood disease.
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PMID:Pathogenesis and treatment of neuroleptic malignant syndrome. 197 19


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