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)

This review considers the evidence for possible involvement of central nervous system pacemaker neurons in several clinical disorders of movement. Two basic types of tremor are discussed from this point of view, i.e., 4--7/sec parkinsonian tremor, of possible thalamocortical origin, and 7--11/sec essential tremor of possible olivo-cerebellar origin. The importance of motor programs and abnormalities in their utilization are considered with reference to the loss of motor function in parkinsonism (? loss of motor programs), and the inappropriate release of such programs as a possible basis for the involuntary movements seen in other movement disorders, such as chorea, athetosis, dystonia, and hemiballismus. The possible role of pacemaker neurons controlling such programs is considered. Finally, the subject of locomotion and the pacemaker model of the spinal locomotor pattern generator for stepping are considered in relation to clinical disorders of gait. While critical evidence is lacking for pacemaker inovlvement in any of these disorders, their possible role is emphasized.
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PMID:Possible involvement of central pacemakers in clinical disorders of movement. 35 Jun 32

In a controlled trial, baclofen (mean dose 45 mg daily) signficantly increased disability from Parkinsonism in 12 patients with the long-term levodopa syndrome. Peak dose choreoathetosis was not improved but benefit was observed in all four patients with "off period dystonia." Adverse side effects were common and severe, and included visual hallucinations, vomiting, and dizziness.
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PMID:Baclofen in Parkinson's disease. 35 2

A dopamine agonist (apomorphine) and a cholinomimetic drug (physostigmine) were administered to five patients with blepharospasm and oromandibular dystonia (Meige disease). The effects of haloperidol and levodopa were also assessed. Apomorphine lessened and physostigmine aggravated the facial dyskinesias in all patients, while placebo injections had no consistent effect. Levodopa did not modify the symptoms, but haloperidol attentuated the facial dystonia. Dysfunction of the basal ganglia, characterized by a state of striatal dopamine preponderance, probably underlies the dystonic spasms in Meige disease. The prominent cholinergic enhancement of facial dyskinesias may distinguish this disorder pharmacologically from tardive dyskinesia, a differentiation which has practical therapeutic implications.
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PMID:Meige disease: striatal dopaminergic preponderance. 37 89

Studies are reported of the variation of melatonin in serum, plasma urine and cerebrospinal fluid in normal subjects and in patients with various diseases. The diurnal variation of plasma and urine melatonin found in healthy controls on a regular dark-sleep pattern persisted when the subjects slept in light. The effect of sleep deprivation and of rapid light exposure at night is reported. There was a correlation between melatonin in morning urine and plasma at 2 a.m. Four hours of extended darkness in the morning as well as a 9-hour shift of sleep and activity cycles following travel affected the melatonin rhythm. The night increase in plasma melatonin preceeded both the cortisol and prolactin rise. A single oral dose of 4.3 X 10(5) nmol of melatonin given to a 44-year-old healthy male gave a peak plasma value of 624 nmol/l after 30 min. Plasma melatonin was not affected by electroconvulsive therapy, TRH-injection, L-Dopa or bromoergocryptine orally. Patients with alcoholism, migraine, postoperative pinealoma, panhypopituitarism, hereditary dystonia and schizophrenics on propranolol exhibited a decreased amplitude of their diurnal rhythm of melatonin. Two patients with pituitary tumors had occasional high levels of plasma melatonin. The change in melatonin secretion in human is apparently controlled by a mechanism which is at least party influenced by environmental lighting conditions, drugs and different disease states.
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PMID:Melatonin in humans physiological and clinical studies. 38 89

Among 25 baboons, Papio papio, 2 consistently showed acute dystonic reactions, with mouthing, compulsive gnawing and limb and trunk dystonia, following the intravenous administration of neuroleptics and related drugs (haloperidol, 0-6-1-2 mg/kg; pimozide 0-5-2-5 mg/kg; chlorpromazine 5-25 mg/kg; metoclopramide 1-5-1-7 mg/kg; oxyperomide 0-25-1-0 mg/kg). The syndrome was not seen after thioridazine (3-7 mg/kg). The dystonic responses occurred within 1-2 h of drug injection and lasted for 2-24 h. They were abolished for 1-3 h within 1-2 min of the intravenous injection of acetylcholine antagonists (benztropine 0-2 mg/kg; hyoscine 0-02 mg/kg). Pre-treatment with a combination of reserpine (2 mg/kg) and alpha-methylparatyrosine (2 X 200 mg/kg) substantially reduced the dystonic response to haloperidol. A second larger dose of haloperidol (5 mg/kg), given 60-90 min after 0-5 mg/kg) initially reduced the intensity of the dystonic response, but after 29 min induced vomiting and generalized seizures in the idiosyncratic baboons. The hypothesis is advanced that the dystonic responses result from release of dopamine on to a sub-population of receptors in the striatum that are relatively insensitive to blockade by neuroleptics.
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PMID:Acute dystonia as an idiosyncratic response to neuroleptics in baboons. 40 64

Haloperidol (0.25 mg/kg i.m.) was injected daily for 6 months in six normal monkeys. Over a 24 hour period, the following symptoms could be observed: akathisia, circling, akinesia, choreoathetoid and dystonic movements, oro-facial dyskinesias and postural tremor with or without harmaline. Six months after cessation of haloperidol, harmaline-induced postural tremor could still be observed in all animals and oro-facial abnormal movements, in one monkey. The neuropathologic study of the experimental material did not disclose any alteration of the central nervous system.
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PMID:Haloperidol-induced dyskinesias in the monkey. 40 96

The authors describe two cases of tardive dyskinesia in which severe axial dystonia and intense facial grimacing produced marked discomfort as well as social and physical disability. Both patients experienced the onset of psychiatric symptoms as young adults, showed a prompt response to antipsychotic drug therapy, and were subsequently left on maintenance treatment for indefinite periods. The severity of this frequently irreversible and disabling condition warrants careful consideration in the use of long-term antipsychotic drug treatment in the young psychiatric outpatient population.
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PMID:Tardive dyskinesia in young adults. 40 2

Fifty patients with the clinical diagnosis of initial manifestations of the deficiency of the brain blood supply and 30 normal persons of the corresponding age (the control group) were studied. The main group consisted of patients from 40-67 years. Along with the similar clinical study rheoencephalographic and electroencephalographic studies with the aid of various functional samples were conducted. The initial manifestations of the inadequacy in the brain blood supply frequently developed on the background of cerebral atherosclerosis of a different type of expressiveness, hypertensive disease and their combination, vegetovascular dystonia. With the help of the functional samples the peculiarities of reactivity of the vascular system were established in these patients. The antiorthostatic and nitroglycerin samples appeared to be informative. The combined REG and EEG registrations demonstrated in these patients signs of a deficit of brain blood supply causing in a number of cases changes in its functional states. The clinical (seldom electrographic) changes are of a reversible character and regress during the treatment of the main vascular disease. The obtained data permit to recommend the method of functional electrography (REG and EEG) in order to reveal the initial forms of brain vascular diseases. These patients must be supervised by a dispansary.
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PMID:[Initial manifestations of cerebrovascular insufficiency (clinico-electrographic studies)]. 41 95

In 82 patients from 20--35 years of age with vegetative-vascular dystonia the authors studied clinical variants of the disease, the bioelectrical brain activity, the state of cerebral circulation, the visual analyzer, the cardiovascular system, histamine, protein, lipid, carbohydrate metabolism and the state of coagulative blood system. In the majority of the cases the studies demonstrated hystaminemia, some shifts in the biochemical blood content, an increased brain vascular tone, a drop of blood repletion and disturbances of regional hemodynamics. The studies also depicted a decreased functional lability of the main cortical bioelectrical processes, disturbances of electric activity and propulsive possibilities of the myocardium. It was also possible to demonstrate intercorrelation between the biochemical and electrophysiological indices with the type and form of the disease. It is assumed that the leading role in the pathogenesis of the disease belongs to the dysfunction of the limbico-reticular complex. Certain recommendations for normalization of the histamine metabolism are given as well as for the normalization of the reticulo-hypothalamic system functions. The authors also indicate a necessity of an early screening of the patients with vegetative-vascular dystonia.
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PMID:[Clinical aspects and pathogenesis of the initial (precrisis) disorders of cerebral circulation]. 41 61

The autosomal recessive inherited disorder glutaryl-CoA dehydrogenase deficiency (glutaric aciduria) runs a progressive course with severe choreoathetosis and dystonia, eventually leading to total helplessness and early death. Theree patients were observed during therapeutic trials with a protein-low diet, riboflavin and GABA analogue. Diet and riboflavin had a slight-to-moderate effect on the clinical symptoms; the excretion of glutaric acid and 2-amino-adipic acid decreased considerably during treatment. Regression of neurologic symptoms was observed during treatment with GABA analogue. It is concluded that the patients should be treated as early as possible with protein-low diet, riboflavin, and GABA analogue.
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PMID:Treatment of glutaryl-CoA dehydrogenase deficiency (glutaric aciduria). Experience with diet, riboflavin, and GABA analogue. 43 Mar 18


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