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 etiology, pathophysiology, diagnosis and clinical presentation, and clinical management of Parkinson's disease are reviewed. The cause of Parkinson's disease, a progressive, degenerative neurologic motor disorder, is unknown. Both endogenous and environmental factors appear to play a role. The clinical features of parkinsonism result from a depletion in dopaminergic transmission in the corpus striatum; the dopamine deficiency is caused by a loss of melanin-containing nerve cells within the substantia nigra and locus ceruleus. In the remaining neurons, hyalin-like masses called Lewy bodies increase in number, but the importance of this is unclear. The diagnosis of Parkinson's disease is based on the clinical presentation of the patient, which initially includes sensory complaints of aching pains, paresthesias, numbness, and coldness. As the disease progresses, the four classic symptoms become prominent: tremor, rigidity, bradykinesia, and postural difficulties. Drug therapy is the cornerstone of clinical management of Parkinson's disease, but no treatment has been found that will retard or reverse the disease. Therapy is usually initiated with anticholinergic agents such as biperiden hydrochloride or trihexyphenidyl hydrochloride with or without amantadine. The mainstay of therapy is levodopa, which is used in combination with dopa decarboxylase inhibitors to decrease the peripheral conversion of levodopa to dopamine. Bromocriptine is a dopamine agonist useful in treating Parkinson's disease. Therapy, which must continue for life, eventually becomes less effective or completely ineffective in all patients. Drug therapy has improved greatly the functional ability of patients with Parkinson's disease, but new agents that can extend the length of effective treatment or reverse the disease are needed.
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PMID:Current concepts in clinical therapeutics: Parkinson's disease. 353 Jun 16

Of 261 patients with clinically diagnosed Parkinson's disease (PD), whose age at the onset was 58.2 +/- 11.3, 46 patients with the onset age above 70 (the mean for the whole group + 1SD) were compared to 44 patients with onset age below 47 (the mean for the whole group - 1 SD). Old-onset PD patient were more susceptible to develop psychotic complications of levodopa treatment. More often had they tremor both as presenting and dominant symptom of their disease. Among young-onset PD bradykinesia was more often the dominant clinical feature, and susceptibility to levodopa induced dyskinesia was higher. In 9 cases of young-onset PD (20.5% of this group) paraesthesia was a presenting symptom, compared to only 1 patient (2%) in the group of old-onset PD.
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PMID:Old-onset Parkinson's disease compared with young-onset disease: clinical differences and similarities. 804 42

In the present study we compared the efficacy and safety of the new dopamine agonist cabergoline (CBG) with bromocriptine (BCR) in Parkinson's disease (PD). CBG has a very long half-life and can be administered as a single daily dose. Forty-four PD patients with uncontrolled motor fluctuations participated in the study. Patients were randomly and blindly assigned to equivalent doses of either CBG or BCR in addition to preexisting levodopa. Dosage was titrated to optimal, using up to 6 mg of CBG or 40 mg of BCR daily. CBG was given as a single morning dose whereas BCR was administered tid. Sixteen patients were followed for 1 year and 16 additional patients for 6 months. The mean follow-up duration was 9 +/- 5 months. The main effect of both drugs was observed on motor UPDRS scores, rigidity, bradykinesia items, and the percentage of awake hours spent during "on" and "off". In general, the effect of CBG was similar to that of BCR. The percentage of awake hours spent during "on" was higher with CBG as compared with BCR. Adverse events included dyskinesias, orthostatism, confusion, edema, and paresthesias in limbs. These effects were seen at similar frequencies with both drugs. The study shows that CBG given as a single morning dose is at least as efficacious as BCR given tid. CBG is a promising dopamine agonist for the treatment of motor fluctuations in PD.
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PMID:Double-blind comparison of cabergoline and bromocriptine in Parkinson's disease patients with motor fluctuations. 879 80

Parkinson syndrome occurs in the course of chemical intoxication, especially Mn, CS2, CO. It is rarely caused by chronic mercury intoxication. We present the case of 55 year old man who was exposed to metallic mercury vapor during 33 years of working in the chemical plant at the production of chlorine. On several occassions patient was removed from contact with Hg because of the symptoms of increased Hg absorption. At the age of 52 he developed hand tremor, balance and gait disturbance with bradykinesia, paresthesias of the upper extremities, neurobehavioral abnormalities, slight memory loss, and spatial disorientation. Psychoneurological examination revealed dementia, Parkinson's syndrome and ataxia of the lower limbs. Mercury excretion in the urine, which equaled 18.3 mu\g creatinine, confirmed exposure to Hg. MRI of the head revealed cortical and cerebellar atrophy. Electroneurography examination found features of subclinical peripheral sensory axonopathy of the upper limbs. Despite atypical clinical course (parkinsonismus) chronic mercury encephalopathy was diagnosed based on documented occupational exposure and diagnostic test results.
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PMID:[Parkinsonism in chronic occupational metallic mercury intoxication]. 1509 29