Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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 In the group of 33 patients 39 could complete the treatment, one patient died suddenly, three had the treatment withdrawn in view of side effects.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

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

Four patients with severe form of Parkinson's disease received transplantation of fetal dopaminergic cells into the caput of the caudate nucleus. The operation was done by an original method using a device designed specially for this purpose. In all cases the duration of the disease was 10 to 15 years, and the predominating signs were tremor, bradykinesia, and markedly pronounced side effects of the treatment (on-off syndrome and involuntary movements). One patients died 5 weeks after the operation. Autopsy demonstrated good survival of the transplanted cells with good integration with the brain of the recipient and traces of positive immunocytochemical reaction for tyrosine hydroxylase. In the other patients a significant clinical improvement was noted after the operation, with reduced intensity of parkinsonian symptomatology, shortening of the duration of the off phase, improved motor ability and reduced intensity of the involuntary movements. The longest follow-up was 24 months.
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PMID:[Transplantation of fetal dopaminergic cells in Parkinson disease]. 140 86

The purpose of this study was to analyze the kinematic properties of upper limb trajectories in Parkinson's disease (PD) patients and to investigate the role of visual feedback from the moving limb. Beyond the characteristic bradykinesia, PD patients differed from controls by generating hand trajectories with asymmetrical velocity profiles that lacked smoothness and were composed of a short initial accelerative phase, followed by a prolonged interval composed of alternating decelerative and accelerative phases. In both groups, the reaction times for movements directed away from the body were longer than for movements directed toward the body; this effect was accentuated in PD. In both groups, initial peak accelerations were significantly larger for distally as compared to proximally directed movements. In the absence of visual feedback from the limb a deterioration in the accuracy of reaching the target was observed in both control and PD patients only for distally directed movements. However, this deterioration and the effect of target location on final accuracy was substantially larger in PD. Taken together, our study suggests that in PD visual information is continuously relied upon for ongoing movement correction, therefore accentuating the bradykinesia. The deficit in final accuracy in the absence of visual feedback reflects the important role played by the basal ganglia in sensorimotor integration.
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PMID:Kinematic analysis of upper limb trajectories in Parkinson's disease. 142 28

Vascular pseudoparkinsonism may be confused with idiopathic Parkinson's disease. Patients may be unnecessarily treated with anti-parkinsonian drugs while their underlying vascular disease is ignored. We investigated 250 parkinsonian patients seen in our Movement Disorders Clinic for a possible vascular etiology. After excluding those with a known secondary cause such as drug-induced parkinsonism, progressive supranuclear palsy, multiple system atrophy and hyperparathyroidism, brain computed tomography and/or magnetic resonance imaging were performed on those who showed poor or no response to levodopa. In those with an ischemic lesion demonstrated on neuroimaging, anti-parkinsonian drugs were stopped and the patients were reassessed. Eleven patients (4.4%) had ischemic brain lesions accounting for their parkinsonism. All were initially diagnosed as Parkinson's disease because of the prominence of bradykinesia and rigidity. Gait disturbance was also common, but resting tremor was distinctly absent. Three anatomical patterns with different prognosis were identified. Three patients with basal ganglia lacunar infarct recovered spontaneously, three with frontal lobe infarcts remained static and five with periventricular and deep subcortical white matter lesions had progressive deterioration. Autopsy in one patient confirmed bilateral frontal lobe watershed infarcts and the absence of brain stem Lewy bodies. Parkinsonian patients with poor or no response to levodopa therapy should be investigated for a vascular etiology.
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PMID:Vascular pseudoparkinsonism. 148 45


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