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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

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

Nocturnal paroxysmal dystonia (NPD) and episodic nocturnal wanderings (ENWs) are complex motor attacks arising abruptly during sleep, especially nonrapid eye movement sleep. NPD is characterized by sudden arousal followed by motor agitation with dystonic posturing, and semipurposeful activity recurring several times per night. When short-lasting, NPD may respond favorably to carbamazepine. ENWs are unusual episodes of ambulation, with unintelligible speech, screaming, and complex, often violent, behavior that responds to anticonvulsants. In both short-lasting NPD and ENWs, electroencephalography may show some evidence of epilepsy; NPD is clinically similar to the frontal lobe seizures that arise mesially or in depth. Paroxysmal arousals (PAs) are even shorter episodes of arousal or awakening during nonrapid eye movement sleep, associated with transient dystonic posturing and related to the short-lasting NPD. PAs, short-lasting NPD, and ENWs probably represent a spectrum of peculiar sleep-related epileptic seizures.
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PMID:Nocturnal paroxysmal dystonia and nocturnal wandering. 163 Jun 41

In recent years, a differentiation has been made between two syndromes that are characterized by brief abnormal paroxysmal movements occurring principally at night: 1, hypnogenic paroxysmal dystonia (HPD), sometimes considered a particular form of dystonia similar to paroxysmal kinesigenic choreoathetosis, and 2, mesiofrontal epilepsy. Whether HPD is a distinct syndrome is not clear. Twenty-three patients, 11 men and 12 women, were hospitalized between 1985 and 1989 for examination of this type of abnormal paroxysmal movements (APM) occurring at night. In order to clarify the physiopathology of these abnormal nocturnal movement as focal epilepsy or a particular form of dystonia, we analyzed the personal and familial antecedents of all 23 patients, the polygraphic records during waking and sleep periods, and the results of neuroradiological examinations. Four patients were examined by positron emission tomography (PET) using i8F deoxyglucose. Symptoms first appeared between 3 and 28 years of age (M, 10.1) and developed over 1 to 20 years (M, 10.1). APM clearly occurred more commonly (greater than 90%) during sleep, usually during phases of slow-wave sleep. The sleeping patient opened his eyes and the motor signs then variously associated affective facial expression; axial postural modifications; tonic, dystonic or choreic postural movements of the limbs; pedalling; automatisms; disordered agitation and vocalization. The seizure was abruptly interrupted after 10 to 60 seconds. There was usually no postictal confusion. Thirteen patients clearly had clear epileptic antecedents: in 9, generalized tonic-clonic seizures; in 4, focal epileptic status. During nocturnal polygraphic recording, 6 patients presented a generalized seizure following a period of APM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Postures and abnormal paroxysmal movements during sleep: hypnogenic paroxysmal dystonia or partial epilepsy?]. 190 68

Eighty-six patients with acute psychotic exacerbations were treated with fixed dosage regimens of oral fluphenazine up to 10-30 mg/day in randomized, double-blind studies. Dystonic reactions occurred in 33.8% of the subjects at risk. Of these, 58% occurred by the third day, 88% by the fourth day, and 100% by the ninth day of treatment; most occurred later in the interdose interval. Significant predictors of dystonic reactions were higher fluphenazine mg/kg dosage and younger age. There was a trend toward a lower risk of dystonia in patients who received amobarbital sodium for agitation. Results are discussed in relation to possible mechanisms of neuroleptic-induced dystonia.
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PMID:Acute dystonia during fixed-dose neuroleptic treatment. 228 8

Administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in primates induced a parkinsonian syndrome that could be reversed by levodopa treatment. Animals quickly developed an apparent restlessness ("akathisia") of the lower limbs after as little as five doses. After 4-10 weeks of regular levodopa therapy, animals developed "peak dose" choreiform movements in the lower limbs that spread, with time, to involve the upper limbs and orofacial musculature. With further treatment (5-21 months), animals developed "peak dose" dystonia that variably involved the limbs and orofacial musculature. These conditions represent novel models of levodopa-induced chorea and dystonia in humans. They depend on the same underlying neuropathology and treatment regimen as their human counterparts. It is to be anticipated that these models of dyskinesia will be useful in determining the mechanisms underlying chorea and dystonia in humans and are ideally suited for experimental evaluation of new treatment strategies.
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PMID:Induction of chorea and dystonia in parkinsonian primates. 229 55

In a prospective randomized and double-blind cross-over study, a new antiemetic regimen consisting of betamethasone (1 x 8 mg) and dixyrazine (a phenothiazine derivative) (4 x 10 mg) was compared with a standard high-dose metoclopramide (4 x 1 mg/kg) schedule for antiemetic treatment in doxorubicin and cisplatin chemotherapy. 100 consecutive patients (62 without prior experience of chemotherapy and 38 with prior experience) entered the study and were followed during 1-4 courses of chemotherapy. Effect and side effect parameters were recorded on questionnaires for patients and nurses using the visual analog scale for quantification. The correlation between the two ways of recording (self-scoring versus recording by nursing staff) was very high, both for effect variables (nausea and vomiting) and the adverse reactions (sedation and extrapyramidal reactions). The median number of courses per patient was 3.0 (range 1-4) and altogether 299 courses were studied. Full emetic protection was achieved in 58% with betamethasone-dixyrazine and in 34% with high-dose metoclopramide regardless of prior patient experience or the cytostatic agents administered. With doxorubicin regimens, betamethasone-dixyrazine gave full protection in 80% compared to 40% for metoclopramide. Cisplatin regimens were a greater challenge and protection against nausea and vomiting was achieved only in 27% with betamethasone-dixyrazine and in 18% with metoclopramide. Adverse reactions were a significant problem with metoclopramide: restlessness 33%, akathisia 19%, parkinsonism 16%, and acute dystonia 3%. Sedation was the same with the two regimens (80%).
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PMID:Betamethasone-dixyrazine combination versus high-dose metoclopramide as antiemetic treatment in doxorubicin and cisplatin chemotherapy. 276 89

Delayed neurological deterioration following anoxia is known to result from carbon monoxide exposure. However, it may also occur with anoxia of other types as well. The present report describes a case of delayed postanoxic encephalopathy with bilateral striatal lesions demonstrated by magnetic resonance imaging. A 27-year-old man exhibited anoxic anoxia caused by upper airway obstruction following general anesthesia for shoulder fracture surgery. Initially he was delirious and markedly excited for one day and became apparently normal for the following three days. Then he relapsed into delayed neurological deterioration with speech and gait disturbance, clumsiness of hand, pyramidal signs and metamorphopsia. Thereafter, he became bed-ridden and fell into semicomatose state with marked motor restlessness, involuntary movement of the tongue and decorticate posture. Twenty-five days later he had a second recovery period after hyperbaric oxygenation that lead to the sequelae with speech and motor disturbances and mild mental changes. I examined the present case as an expert witness in a civil suit eleven years after initial anoxia. The patient showed slight intellectual impairment and personality change. Impairment in figure-ground differentiation and disorders of spatial thought were also observed. Neurological examination revealed anisocoria, dysarthria with acquired stuttering, disturbances of fractionated movement of fingers, writer's cramp and Babinski's sign bilaterally. Postural dystonia of both hands and fingers, rigidity and spasticity of all extremities were also present. Magnetic resonance imaging (MRI) showed bilateral lesions of the corpus striatum, especially of the putamen. Some portion of the caudate nucleus was also involved. Cerebral cortices and white matter were slightly atrophic. From the above clinical course and neurological findings, we diagnosed the present case as delayed postanoxic encephalopathy. Ginsberg (1979) noted that in cases of anoxia not related to carbon monoxide, diffuse demyelinative changes of cerebral hemispheral white matter tended to be associated with relapsing clinical course, and gray matter injury was only seen in a few cases. MRI findings in the present case suggest that main site of the lesion to be in gray matter of the corpus striatum. In this respect, the present case is considered to be noteworthy.
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PMID:[A case of delayed postanoxic encephalopathy with bilateral lesions of the corpus striatum]. 281 6

Movement abnormalities in neuroleptic-treated, psychiatric patients are classified as (a) initial syndromes, including dystonia, parkinsonism, and hyperkinetic abnormalities such as initial dyskinesia (ID) and akathisia, all of which are related to the neuroleptic dose and can be considered as overdose phenomena; (b) tardive syndromes, mainly the classic tardive dyskinesia (TD) syndrome, more seldom tardive akathisia and tardive dystonia, which may all develop or aggravate after withdrawal of neuroleptic treatment; and (c) age-related, spontaneous dyskinesia, akathisia, and dystonia, and schizophrenia-related, hyperkinetic, often stereotyped, movements and restlessness. ID and TD can occur simultaneously, and may depend, at least partially, on identical mechanisms. The pathophysiology of TD is still not clear, and the traditional dopamine (DA) hypersensitivity model seems inadequate. Animal experiments suggest that blockade of some DA receptors in the brain (e.g., in ventromedian striatum) may counteract hyperkinesia and produce parkinsonism, while a concomitant blockade of other similar receptors in other brain regions (e.g., in anterodorsal striatum) may aggravate movements. This offers an explanation for the concomitant occurrence of parkinsonism and hyperkinetic movement abnormalities (ID and akathisia) relatively early in a neuroleptic treatment, and may also contribute to the understanding of the pathophysiology of TD. It is concluded that pathophysiologically TD is a heterogeneous syndrome depending on a subtle balance between several neurotransmitters in the brain, including DA receptor blockade and hypersensitivity of DA and GABA receptors.
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PMID:Pathophysiological mechanisms underlying tardive dyskinesia. 286 Jun 66

In a prospective study, the intensity of extrapyramidal symptoms (EPS) was rated in two groups of delirious, medically ill patients. Fourteen patients received intravenous (IV) haloperidol and benzodiazepines for control of severe agitation and four received IV haloperidol alone. Patients were rated daily by a standardized scale for EPS by raters blind to the dose of haloperidol and benzodiazepines. Patients receiving haloperidol and benzodiazepines had significantly (p less than 0.001) less EPS than patients receiving IV haloperidol alone. In the haloperidol and benzodiazepine group there were only one case of very mild parkinsonian-like EPS and no cases of akathisia or dystonia. No adverse respiratory or cardiac reactions were seen in any patients. The literature on the use of IV haloperidol alone and in combination with benzodiazepines is briefly reviewed and possible explanations of the lower intensity of EPS with IV haloperidol in combination with benzodiazepines are discussed.
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PMID:Controlled study of extrapyramidal reactions in the management of delirious, medically ill patients: intravenous haloperidol versus intravenous haloperidol plus benzodiazepines. 289 42


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