Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0233565 (bradykinesia)
 2,352 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The occurence of extranuchal dystonia, facial spasm, parkinsonian symptoms (facial masking, bradykinesia, rigidity), tremor and family history of tremor was tabulated in a group of 30 patients with IST. The incidence of extranuchal dystonia increased as severity of IST increased. There was a strong trend for severity of extranuchal dystonia to increase as severity of torticollis increased, which was significant (p less than 0.001). There was a similar trend for severity of facial spasm to increase with increasing severity of torticollis (p less than 0.025). Parkinsonian features were seen in 10 of 30 patients, and in three the diagnosis of Parkinson's disease could be entertained. Tremor was seen in 26 of 30 patients being mild in 12, moderate in 11, and severe in three. A family history of tremor was present in 16 of 28 cases for whom history was available (12 primary, four secondary relations). The results are most consistent with the hypothesis that IST is a variant of DMD with tremor as an integral part of the disease and tremor represents a forme of the disease in family members.
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PMID:Dystonia and tremor in spasmodic torticollis. 94 73

Bromocriptine in high doses (up to 100 mg per day) was administered to 14 patients with advanced Parkinson's disease whose disorder was progressing despite optimum treatment with levodopa combined with a peripheral dopa decarboxylase inhibitor (carbidopa). In 10, bromocriptine (mean dose, 57 mg) induced a statistically significant (P less than 0.01) improvement in rigidity, tremor, bradykinesia, gait disturbance and total score. In seven patients levodopa with carbidopa was completely replaced by bromocriptine (mean dose, 70 mg), with improvement in four. Adverse effects were similar to those observed with levodopa and carbidopa, except that in individual patients abnormal involuntary movements and diurnal oscillations in performance (on-off effect) were decreased whereas orthostatic hypotension and mental changes were increased. Bromocriptine appears to be a major new agent in Parkinson's disease that is especially promising in patients no longer responding to levodopa.
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PMID:Treatment of parkinson's disease with bromocriptine. 98 85

On the basis of a reassessment of the aetiopathogenetic problem and the neuroendocrine implications, the therapeutic effectiveness of a prolactin inhibitor, 2-alpha-Br-ergocryptine (CB 154), in Parkinson's disease is assessed. Five patients were treated for a total of two weeks using doses between 10 and 15 mg/die. CB 154 was found to act as a dopaminergic receptor agonist at nigro-striatal level, considerably improving tremor and rigidity and to a lesser extent bradykinesia and total disability.
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PMID:[Neuroendocrine aspects of Parkinson's disease. Therapeutic/effect of a prolactin inhibitor]. 103 12

Nine patients with Parkinsonism were studied before and after treatment with piribedil, a dopamine-receptor stimulator. Piribedil appeared to have a slight anti-Parkinsonism effect upon bradykinesia, and possibly upon tremor, but did not improve rigidity. The chief toxic effects were drowsiness and confusion, and two patients experienced nausea. Changes in homovanillic acid in the cerebrospinal fluid indicated that the drug reduced the turnover of endogenous dopamine. In spite of this definite neuropharmacological action, no clear-cut associated clinical benefit was demonstrated. The significance of these findings is discussed.
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PMID:Clinical and pharmacological evaluation of the effects of piribedil in patients with parkinsonism. 109 Nov 22

In 38 patients with Parkinson's syndrome Madopar preparation was used (L-dopa with peripheral decarboxylase inhibitor) in 33 cases as the main drug and in 5 cases as an addition to L-dopa. In the group of 33 patients 39 could complete the treatment, one patient died suddenly, three had the treatment withdrawn in view of side effects. The effectiveness of Madopar was assessed by means of five-rate scoring systems NUDS and ART. Clinical improvement was found in 22 cases (about 67%). The improvement included mainly bradykinesia and rigidity, while tremor was only slightly improved. Side effects developed in about 40% of patients and were slight and transient (apart from 3 cases). The main contraindications seem to be psychotic disturbances. In the group of 5 cases treated with Madopar as an additional drug in low doses improved the result of long-term treatment with L-dopa.
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PMID:[Treatment of parkinsonism with L-dopa and peripheral decarboxylase inhibitor]. 116 36

Judgment of the visual vertical and horizontal in the upright body position was abnormal in 19 (29 percent) of 66 patients with Parkinson's disease. The magnitude of errors correlated with the degree of rigidity and of tremor in the limbs, but not with bradykinesia or other clinical features. The results suggest that the effect on visual perception of the vertical and horizontal coordinates in patients with parkinsonism is brought about by specific changes in the basal ganglia and is not, as in the case of other visual-motor tasks, determined merely by the overall severity of cerebral pathology.
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PMID:Judgment of the visual vertical and horizontal in patients with Parkinsonism. 116 8

On the basis of observations of 18 patients the authors evaluated clinically the action of Sinement preparation (Merch, Sharp and Dohme) containing L-dopa 250 mg and carbidopa 25 mg in the treatment of Parkinson's disease. In the evaluation particular attention was given to side effects. Therapeutic results of Sinemet and L-dopa alone were compared in patients receiving these drugs alternatively. The observations of authors indicate that Sinemet gives the same therapeutic results as L-dopa, but in much lower doses and with less frequent side effects. Sinemet, similarly as L-dopa exerts the best effect on bradykinesia and muscular rigidity and less on tremor.
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PMID:[Comparison between results achieved by administering L-dopa and Sinemet in parkinsonism in the light of our records]. 118 52

We report an autopsied case of Parkinson's disease manifesting Shy-Drager syndrome. At the age of 63 years, the patient noticed an onset of progressive orthostatic dizziness, which was followed by constipation, dysuria, and sexual impotence. When he was 66 years old, syncopal attack for a few minutes, tremor in the bilateral hands, and memory disturbance developed. On admission, his blood pressure was 142/72 mmHg in supine position, which fell to 58/42 mmHg on standing with appropriate increase of heart rate. Neurological examination revealed hallucination, memory disturbance, masked face, muscular rigidity, bradykinesia, mild postural tremor, and autonomic dysfunction including severe orthostatic hypotension, hypohydrosis, constipation, dysuria, and sexual impotence. Electroencephalogram showed diffuse slowing. Brain CT demonstrated absence of severe atrophy of the cerebellum, and brain stem. Pharmacological study revealed denervation hypersensitivity to the intravenously administrated noradrenaline. A diagnosis of Shy-Drager syndrome was made, and he was treated with anti parkinsonian drugs. However, no improvement was observed in his clinical symptoms. Seven months later, he died of pneumonia. Neuropathological examination revealed marked neuronal cell loss and gliosis in the substantia nigra and locus ceruleus. Lewy bodies were seen in those pigmented nuclei, dorsal vagal nucleus, hypothalamus and nucleus basalis of Meynert. No abnormality was found in the intermediolateral nucleus of the spinal cord. This is the first report on a Japanese patient who presented clinically Shy-Drager syndrome and pathologically typical Parkinson's disease. In this patient, from the pharmacological and pathological findings, sympathetic ganglia were supposed to be the responsible lesion for orthostatic hypotension.
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PMID:[An autopsied case of Parkinson's disease manifesting Shy-Drager syndrome]. 130 25

Ethylene oxide is a gas widely used in the production of industrial chemicals. It is also used to sterilize heat-sensitive medical supplies. Previous reports of acute and chronic exposure have described neurotoxic effects like peripheral neuropathy and cognitive impairment. We describe a pure parkinsonian syndrome following acute ethylene oxide intoxication. A 39-years-old male was referred to our Movement Disorders Clinic for evaluation of a parkinsonian syndrome. He was acutely exposed to ethylene oxide four years before and remained comatose for three days, and gradually regained consciousness. At that time he showed a global parkinsonian syndrome including bradykinesia, rigidity and rest tremor, with a severe motor disability; no other neurological disorders were found. The symptomatology was partially controlled with biperidene and levodopa plus carbidopa. Two years later he developed L-dopa induced dyskinesias. Four years after the intoxication he was evaluated at our clinic. General examination showed no abnormalities. Neurologic examination revealed a normal mental status. Motor evaluation disclosed moderate bradykinesia, rigidity and rest tremor, shuffling gait, poor facial mimic, stooped posture, and his speech was low and monotonous; deep tendon reflexes were brisk. The Hoehn-Yahr disability score was degree IV. Routine laboratory and radiological exams showed results within normal limits. The CSF examination was normal. Brain computed tomography and magnetic ressonance were normal. A trial with bromocriptine and levodopa plus carbidopa did not improve dyskinesia, and he was put on a schedule including amantadine and biperidene with improvement to grade III in Hoehn-Yahr scale. In the present case there was a clear relation between the acute exogenous intoxication and irreversible parkinsonism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Parkinsonism secondary to ethylene oxide exposure: case report]. 130 62

Treatment of Parkinson's disease (PD) can be divided into two categories: symptomatic therapy (restoring dopamine levels toward normal and reversing functional disability) and preventive therapy (interfering with the pathophysiologic mechanism of PD to prevent or decrease the rate of progression of the disease). Regarding symptomatic treatment, although anticholinergic preparations generally are considered effective for the symptoms of tremor and rigidity without altering bradykinesia, their effectiveness is limited and adverse reactions are common; their role should be restricted to use as adjuvants to levodopa therapy. Amantadine has been shown to be as effective as anticholinergics, but it lacks long-term efficacy. Dopamine agonists--bromocriptine, pergolide mesylate and lisuride in Europe--are not as effective as levodopa and therefore rarely are used as initial therapy; their proposed role, too, is as adjuvants to levodopa therapy. Levodopa is the most effective drug presently available for the treatment of PD; its introduction is accompanied by rapid and dramatic reduction of symptoms and signs. Initial adverse reactions are not usually a major problem; and although there is speculation that initiation of therapy should be delayed because of possible long-term complications, clinically distinguishing these from problems related to disease progression itself is difficult. The possibility that nigral cell death is mediated by oxidative mechanisms provides the basis for considering antioxidant therapy as protective treatment; selegiline, an antioxidant, has been found to delay the need for symptomatic therapy. It is suggested that initial treatment of Parkinson's disease begin with both preventive therapy with selegiline and symptomatic treatment with the sustained-release preparation of levodopa, which may be associated with fewer long-term complications.
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PMID:Initiating treatment of Parkinson's disease. 134 9


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