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)

In the past, stereotactic surgical intervention for Parkinson's disease was considered indicated only in those patients with active motor manifestations that were refractory to pharmacological therapy, manifestations such as tremor, rigidity, dystonia, and dyskinesia. With the reintroduction and refinement of Leksell's posteroventral pallidotomy, both akinetic and hyperkinetic symptoms are now amenable to surgical treatment. We have analyzed the results of 126 patients who underwent either unilateral (n = 58) or bilateral (n = 68) posteroventral pallidotomies. The Unified Parkinson's Disease Rating Scale and Hoehn and Yahr Staging Scale were used for preoperative and postoperative objective assessments. Postoperative follow-up evaluation occurred initially at 1 week and subsequently at intervals between 1 and 12 months (mean = 4.5 months) after surgery. Although individual motor subscores on the Unified Parkinson's Disease Rating Scale were significantly reduced (n = 126, P < or = 0.01), the most dramatic findings were the reversal of akinetic symptoms and the elimination of dyskinesia and profound "off" periods. These clinical results, combined with intraoperative microelectrode records revealing pallidal neuronal hyperactivity, suggest a reconsideration of the pathophysiology of akinesia and point to possible mechanisms of akinesia improvement by posteroventral pallidotomy in some parkinsonian subgroups.
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PMID:The results, indications, and physiology of posteroventral pallidotomy for patients with Parkinson's disease. 764 96

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

Motor disorders affecting the orofacial musculature include bruxism, chronic orofacial muscle pain affecting the jaw and neck muscles and the involuntary waking period disorders such as orofacial dyskinesia, oral mandibular dystonia, tremor and others. Research at UCLA has touched these and many other areas. Current results have indicated the usefulness of contingent afferent electrical stimulation of the lip to control bruxism; provided information regarding the fatigue, endurance and recovery faculties of the protrusive jaw muscles; explored the issue of chronic muscle hyperactivity inducing headache pain; and worked with botulin toxin as a method to treat orofacial dystonia and dyskinesia.
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PMID:Oral motor disorders in humans. 768 5

While dyskinetic movements have been reported in primates with unilateral excitotoxic lesions following stimulation by dopaminergic agonists, the presence and intensity of the dyskinetic syndromes have varied extensively with size and location of lesion. With the intent of producing a more reliable behavioral model of Huntington disease, anatomically-defined lesions of limited size were produced by magnetic resonance imaging-guided stereotaxic injection of quinolinic acid in specific regions within the caudate and putamen of rhesus monkeys. The location and extent of the lesions were verified by magnetic resonance imaging as well as quantitative positron emission tomography imaging with the dopamine D1 specific receptor ligand SCH 39166 as a marker for striatal output neurons. The quality, frequency and duration of dyskinetic movements were assessed and quantified before and after administration of 0.5 mg/kg apomorphine in multiple test sessions over several months. Selective unilateral lesions in the posterior putamen, but not in the anterior putamen or the head of the caudate, produced marked dystonia and dyskinesia after apomorphine administration. While combined unilateral lesions of the caudate and posterior putamen produced dyskinesia similar to selective posterior putaminal lesions, combined unilateral lesions of the anterior and posterior putamen did not elicit dyskenesia. On the basis of these results, one monkey received a bilateral selective lesion in the posterior putamen. This animal remained healthy and exhibited marked spontaneous Huntington-like chorea spontaneously in the first 48 h after lesioning and persistent apomorphine-induced dyskinesia thereafter. We conclude that bilateral selective excitotoxic lesions of the posterior putamen provide an improved model of the movement disorder of Huntington disease.
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PMID:Selective putaminal excitotoxic lesions in non-human primates model the movement disorder of Huntington disease. 775 72

Eight Cebus apella monkeys previously exposed to D1 and D2 antagonists were treated subcutaneously for 8 weeks with the D1 antagonist NNC 756 (0.01 mg/kg), followed by a wash-out period of 4 weeks and treatment with the D2 antagonist raclopride for 8 weeks (end doses 0.01 mg/kg). NNC 756 induced no dystonia, while marked dystonia was induced by raclopride. Mild tolerance to the dystonia-inducing effect of raclopride slowly developed. Both drugs induced significant sedation and mild bradykinesia. Sedation induced by NNC 756 was stronger than that of raclopride, while no differences were found regarding bradykinesia. The sedative effect of both NNC 756 and raclopride increased over time during chronic treatment. No changes in bradykinesia developed. No significant dyskinesia was induced by NNC 756, while raclopride significantly induced both acute and tardive oral dyskinesia. Furthermore, raclopride-induced acute dyskinesia worsened during chronic treatment. Concomitant treatment with NNC 756 tended to reduce the D1 agonist SKF 81297-induced dyskinesia and grooming, while concomitant treatment with raclopride increased SKF 81297-induced dyskinesia and tended to decrease SKF 81297-induced grooming. Chronic treatment with raclopride induced supersensitivity to both the D2/D3 agonist LY 171555 and SKF 81297, while chronic NNC 756 treatment only induced supersensitivity to SKF 81297. The findings indicate that D1 antagonists may induce less dystonia and oral dyskinesia as compared with D2 antagonists and support the hypothesis of both a permissive and an inhibitory interaction between D1 and D2 receptor systems.
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PMID:Long-term treatment with low doses of the D1 antagonist NNC 756 and the D2 antagonist raclopride in monkeys previously exposed to dopamine antagonists. 785 8

A double-blind, randomized study of parallel group design comparing remoxipride and thioridazine (dose range 150-600 mg/day of either drug) was undertaken at 11 Australian centres. A total of 144 patients (remoxipride = 73, thioridazine = 71) with DSM-III-R schizophrenia or schizophreniform disorder commenced the study, and 89 patients (remoxipride = 45, thioridazine = 44) completed the 6 weeks of the trial. The mean daily doses at last rating were 404 mg (remoxipride) and 378 mg (thioridazine). Initial Brief Psychiatric Rating Scale scores decreased by a mean 8.7 points in both remoxipride and thioridazine groups. Equivalent treatment responses were also confirmed by Clinical Global Impression. During the study, sedatives or hypnotics were needed by 68% of the remoxipride patients and 51% of the thioridazine patients. Thioridazine was associated with more postural hypotension, drowsiness, increased sleep, headache, dizziness on rising, dry mouth, sexual dysfunction and weight gain, while remoxipride patients reported more insomnia. There were no differences between remoxipride and thioridazine on dystonia, hypokinesia, dyskinesia, rigidity and akathisia. The results indicate that remoxipride has similar antipsychotic efficacy to thioridazine but causes fewer side effects.
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PMID:The Australian multicentre double-blind comparative study of remoxipride and thioridazine in schizophrenia. 787 41

HPD is a clinical entity characterized by childhood-onset postural dystonia, which shows marked diurnal fluctuation (aggravation of symptoms towards evening and their alleviation in the morning after sleep), and dramatic and sustained response to levodopa without any adverse effects, such as wearing-off or dyskinesia. Since the first report by Segawa et al. (1971), many cases have been reported under the title HPD or related nomenclature. In this review, we describe details of clinical features and recent laboratory studies of HPD, to differentiate it from other disorders manifesting dystonia in childhood. It has been suggested that HPD has a genetically determined abnormality, being restricted to the terminals of the nigrostriatal dopaminergic neurons, which results in reduced dopamine content.
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PMID:[Hereditary progressive dystonia with marked diurnal fluctuation (HPD)]. 790 89

Parkinsonian symptoms and levodopa-induced dyskinesias (LIDs) are often considered to occur first, and to predominate, in the upper limbs. We studied the topography, type, sequence, and severity of LIDs in 20 consecutive patients with Parkinson's disease (PD) experiencing LIDs for less than 6 months (Hoehn and Yahr stage II-III; average age at onset of PD, 57 years; average duration of PD, 7.2 years; percent of improvement with levodopa > 50) and compared them with the initial site, form, and evolution of the patient's motor disability. Parkinsonism started in the foot in six of 20 patients. Motor disability in the "off" state was similar in upper and lower extremities, except for akinesia, which was worse in the lower limbs. A careful interview indicated that LIDs had started in the foot in all patients. After administration of a single dose of levodopa ("levodopa test"), LIDs appeared in all patients as dystonia of the foot homolateral to the side most affected by PD (onset-of-dose dyskinesia). LIDs were preceded by "off" dystonia (dystonic foot) in six patients and were followed by mid-dose dyskinesia in eight. This is consistent with an early loss of dopaminergic innervation corresponding somatotopically to the foot area. The similarities among initial LIDs, early morning dystonia, and onset-of-dose dyskinesia suggest a similar pathophysiology.
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PMID:Do parkinsonian symptoms and levodopa-induced dyskinesias start in the foot? 793 84

Dyskinetic syndromes are conditions with involuntary movements. They can have different causes, but are often due to dysfunction of the basal ganglias. The clinical picture varies but all show spontaneous alterations in intensity as well as deterioration with stress. This often leads to misjudgment of cases of dyskinesia. It is however important to be aware of these syndromes as medical treatment is effective in many cases. The treatment of tremor, tics, chorea, myoclonus, dystonia and medically induced dyskinesia is reviewed and the clinical pictures are briefly described.
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PMID:[Treatment of dyskinetic syndromes]. 799 12

Dyskinetic syndromes are conditions with involuntary movements. They can have different causes, but are often due to dysfunction of the basal ganglias. The clinical picture varies, but all show spontaneous alterations in intensity as well as deterioration with stress. This often leads to misjudgement of cases of dyskinesia. It is however important to be aware of these syndromes as medical treatment is effective in many cases. The treatment of tremor, tics, chorea, myoclonus, dystonia and medically induced dyskinesia is reviewed and the clinical pictures are briefly described.
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PMID:[Treatment of dyskinetic syndromes]. 799 72


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