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)

We studied 115 Japanese patients with idiopathic cranial dystonia (Meige disease), using surface electromyography (EMG) focused on the orbicularis oculi muscles to classify the findings of the abnormal involuntary movements of this disease and to evaluate the pathophysiology of blepharospasm (BS). Surface EMGs at rest and at voluntary eyelid opening after eyelid closing were investigated. We found 62 (53.9%) patients exhibiting the overblinking type, 37 (32.2%) the tonic BS type, and 16 (13.9%) the normal type of behavior, considering the frequency of spontaneous blinking and presence of spasms. The present results suggest that BS is not a summation of blinking but a spatial and temporal extension of the orbicularis oculi muscle activity engaging in blinking, and the classification of the present study can support the investigation of the temporal characteristics of patients with this disease.
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PMID:Surface electromyographic study of idiopathic cranial dystonia focused on the orbicularis oculi muscles. 150 71

Dystonia refers to a specific clinical entity as well as movements occurring as a result of other syndromes. Dystonic movements are the most commonly misdiagnosed abnormal involuntary movements. Dystonia worsens under emotional or physical stress and with fatigue, lessens with rest, relaxation, hypnosis and sensory tricks, can have diurnal fluctuations and may disappear in sleep. Dystonia is often confused with chorea and myoclonus and considered to be voluntary, that is, psychogenic in origin, in part because of its unusual and varied clinical expression. The neuroscience nurse, cognizant of the natural history, phenomenology and genetics of dystonia, will be able to identify early signs and symptoms, inform colleagues and teach family members who care for children with primary dystonia.
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PMID:The primary dystonias of childhood. 183 82

Intermittent treatment with L-dopa over a 2-year period induced abnormal involuntary movements in MPTP-treated squirrel monkeys. Dyskinesias included a choreic and dystonic component. Dose-response curves for chorea and dystonia revealed that the same dose of L-dopa (30 mg/kg) induced the highest score for both dyskinesias: however, the severity was much greater for chorea. Choreic movements were always most prevalent at the time of peak effect, whereas dystonia was apparent at the time of peak effect and at "end-of-dose", and was occasionally observed spontaneously. Our findings indicate that squirrel monkeys treated with MPTP develop L-dopa-induced dyskinesias which closely resemble those observed in Parkinson's disease. This species provides a valuable animal model to develop improved therapeutic agents.
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PMID:Characterisation of dyskinesias induced by L-dopa in MPTP-treated squirrel monkeys. 239 4

Movement disorders are usually of central origin, but sometimes involuntary movements occur after peripheral trauma. Twenty eight patients, 13 women and 15 men, mean age 37 years (range 15-78), were studied with dystonia or tremor in whom the onset of abnormal movements was related, in time and in distribution, to injury of a body part. Among 23 patients with latency of less than one year after injury, focal dystonia of the involved body part was found in 18, nine of whom had associated reflex sympathetic dystrophy (RSD). One of five patients with peripherally induced tremor had RSD. Abnormal electromyography or nerve conduction velocities were found in the affected limb in four patients, but other electrophysiologic techniques provided evidence for disturbed central function. In 15 patients (65%) possible predisposing factors may have contributed to the pathogenesis of the trauma induced abnormal involuntary movements.
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PMID:Dystonia and tremor induced by peripheral trauma: predisposing factors. 322 Dec 19

Mean-age of onset of Parkinson's disease is 56 years. The older the patient is the more rapid is on average the progression of disability. In the early phase the motor symptoms respond well to therapy. Later, variations of response to therapy and side-effects of therapy occur (wearing-off, end-of-dose akinesia, end-of-dose dystonia, dopaminergic abnormal involuntary movements, pharmacogenic psychoses etc.). Due to the modern pharmacologic treatment of Parkinson's disease with dopaminergic substances disabling stages of the disease occur mean 3 to 5 years later than before levodopa-substitution was initiated. The incidence of depression, distinct cognitive deficits (impairment of memory, visuospatial deficits) and dementia increases in the course of the disease. The tremulous form of Parkinson's disease generally leads to less motor impairment than the rigid-akinetic form. Parkinson's disease of early onset (onset before the age of 40), may be regarded as a subtype of Parkinson's disease. Benign and malignant types of Parkinson's disease may be distinguished, as well as overlaps with multisystem atrophies.
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PMID:Nosography of Parkinson's disease. 346 66

15 years' experience with Parkinson's disease treated with levodopa was compared to the 15 years before the advent of levodopa. Progression to severe disability and death was prolonged, at each stage of severity, by 3 to 5 years. At each duration of illness, the percentage of patients with severe disability was reduced significantly. There was some indication that independence was prolonged by early treatment. Life expectancy was increased to approximately that of the unaffected population. However, especially with patients with onset of disease before the age of 50, fluctuations of therapeutic response and severe abnormal involuntary movements interfered with satisfactory therapeutic results. Supplemental bromocriptine produced a smoother therapeutic response and decreased "off" period dystonia and leg pains in over 70% of patients. At dosages below 20 mg daily, it was not particularly effective in severely affected disabled patients. Adverse reactions prevented the use of bromocriptine in less than 20% of patients.
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PMID:Result of chronic levodopa therapy and its modification by bromocriptine in Parkinson's disease. 398 85

Arteriovenous malformations have only rarely been implicated as a cause of basal ganglia dysfunction. In four instances where such a lesion was uncovered, abnormal involuntary movements were present. In two, tremor involving the contralateral limbs occurred, while in others the head and neck were involved in dystonic movements and posture. The clinical and angiographic characteristics of these four patients have been assessed and are presented in detail in this report. The possible mechanism by which arteriovenous malformations may disturb the internal circuitry of the basal ganglia and induce symptoms are discussed.
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PMID:Extrapyramidal dysfunction with cerebral arteriovenous malformations. 482 31

The "off" painful dystonia (OPD), usually concerning the feet, is a type of abnormal involuntary movement, induced by the chronic use of levodopa. It is mostly observed in the advanced stage of Parkinson's disease (PD), particularly in the early morning, in the evening, and late at night. Indeed, some patients have experienced OPD also during "on" periods when dystonic posture of the foot alternates with dyskinesia. The pain probably is due to sustained muscle contraction, which causes prolonged muscle spasm, as in primary dystonia or torticollis. Dopaminergic drugs like bromocriptine, pergolide, and especially apomorphine (s.c. infusions, or bolus), can dramatically improve the OPD. Anticholinergics baclofen and lithium are alos used in the management of OPD with some benefit. On the other hand, clinical experience shows that in many cases, these therapeutic procedures are not always enough to produce the expected results. Thirty PD patients (22 men and eight women) with OPD of the foot were treated with botulinum toxin (Botox, Btx) using electromyograms to guide injections. Dystonia was evaluated using a quantitative rating scale. The selection of the muscles for Btx treatment was carried out on the basis of foot posture. We injected Btx into tibialis posterior, tibialis anterior, gastrocnemius, flexor digitorum longus, and extensores hallucis longus with a median dose 40 IU for each muscle, distributed in two sites. In all patients, the pain improved within 10 days, whereas in 21 patients, the pain disappeared completely for 4 months (range, 3-7 months); a concomitant improvement in intensity of the dystonic spasm was also observed. No side effects were reported. Seven patients with associated "on" foot dystonia described an improvement of foot posture on walking. In conclusion, in this uncontrolled study, the use of Btx in OPD seemed a promising tool to improve pain linked to foot dystonia; however, because of the well-known underlying dopaminergic defect in OPD, the Btx therapy should be considered only if the dopaminergic treatment established for the management of OPD has failed.
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PMID:"Off" painful dystonia in Parkinson's disease treated with botulinum toxin. 765 52

A variety of inheritable metabolic disorders produce movement disorders. A lists of conditions associated with tremor, athetosis, chorea, dystonia and myoclonus are presented as a guide for the differential diagnosis of such abnormal involuntary movements. The list includes aminoacidopathies, lipidoses, mucopolysaccharidoses, mucolipidoses, organic acidemias, mitochondrial cytopathies and disorders of carbohydrate, purine, and metal metabolism. Clinical, pathological and biochemical features of movement disorders of three typical examples, Wilson's disease, Lesch-Nyhan syndrome and glutaric acidemia type 1, are described.
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PMID:[Movement disorders in miscellaneous disorders--inherited metabolic diseases]. 827 72

Chronic electrical subthalamic nucleus (STN) stimulation is under investigation for alleviating parkinsonian symptoms. STN alterations may carry the risk of provoking abnormal involuntary movements (AIMs). We took advantage of the reversibility of the stimulation technique to assess the possibility of inducing AIMs, using different electrical variables with or without concomitant levodopa intake. Above a given threshold voltage, stimulation could induce contralateral distal mobile AIMs or hemiballism in the off-drug condition in two patients. AIMs occurred after a latency that varied from a few minutes up to several hours after switching on the stimulator. Hemiballism immediately disappeared upon switching off the stimulator. In these patients, levodopa had never provoked that type of AIMs before surgery. Levodopa-induced AIMs were not modified by electrical stimulation, but off-phase dystonia disappeared in one patient. Stimulation of the STN induced AIMs that resembled both those observed following spontaneous lesions of the STN and levodopa-induced diphasic AIMs in parkinsonian patients. As electrical stimulation provoked AIMs and antiparkinsonian benefit occurred with different electrical variables and different timing, the mechanisms responsible for these two effects could be distinct.
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PMID:Abnormal involuntary movements induced by subthalamic nucleus stimulation in parkinsonian patients. 872 37


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