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)

Seventeen patients with either Parkinson's disease or post-encephalitic parkinsonism were treated with Piribedil, an apomorphine-like drug, in single blind conditions for a period ranging from five weeks to twenty-four months. The analysis of the results shows that Piribedil modifies the extrapiramidal symptomatology being specially effective against the tremor either when used alone or in association with L-Dopa. The side effects noticed during treatment with Piribedil are similar to those of Apomorphine, and are dose-dependent.
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PMID:[Piribedil in the treatment of Parkinson disease (author's transl)]. 77 98

After the stereotactic treatment of patients with Parkinson's disease, a correlative study between the site of the deep subcortical lesions and subsequent cerebellar signs (dysmetria and hypotonia) was made. Cerebellar signs appeared in 27 cases (40.8%) of subthalamotomy and in 3 cases (8.6%) of VIM thalamotomy 2 weeks after an operation. The appearance of these signs after an operation was independent from the operative effect on tremor. Thus, we concluded that VIM thalamotomy might be better than subthalamotomy for the relief of tremor in Parkinson's disease.
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PMID:Slight cerebellar signs in stereotactic thalamotomy and subthalamotomy for parkinsonism. 80 61

A double-blind, placebo-controlled, crossover study with long-term follow-up of amantadien i- Parkinson's disease was performed on 26 patients. Other antiparkinsonian medications were discontinued in all but three patients. Amantadine resulted in a statistically significant 12 percent overall improvement over placebo. Twenty of 26 patients, without breaking the code, selected amantadine for long-term usage. Ten patients continued treatment for 10 to 12 months, and an overall statistically significant improvement was noted at 2 weeks and at 1, 2, 3, and 10 to 12 months. Improvements in tremor and rigidity remained relatively constant, while there was some apparent loss of efficacy in timed tests and quality of timed tests. Amantadine appears effective in the long-term treatment of some patients with Parkinson's disease.
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PMID:Amantadine in Parkinson's disease. A double-blind, placebo-controlled, crossover study with long-term follow-up. 80 67

The antiparkinsonian activity of bromocriptine, a presumed dopaminergic receptor agonist, was investigated in monkeys with surgically induced tremor and in a group of parkinsonian patients. A single administration of bromocriptine resulted in a dose-dependent relief of tremor in monkeys. Repeated administration enhanced this effect. Only mild abnormal involuntary movements were observed and only after repeated administration. Eleven patients with Parkinson's disease were treated with bromocriptine (mean dose, 26.4 mg a day). Clinically obvious improvement was noted in one or more of the cardinal signs of the disease in six patients (responders). No obvious improvement in any of the cardinal signs was noted in the remaining five patients (nonresponders). Clinically, the responders were older and more severely affected and had been on a higher dose of levodopa. However, they had had the disease for a shorter period. It is suggested that failure to respond to bromocriptine may be related to a decrease in the sensitivity of postsynaptic dopaminergic receptors.
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PMID:The antiparkinsonian efficacy of bromocriptine. 81 21

The clues vary, and many of the "typical" signs are misleading or even contradictory. One patient acts impetuously while another seems to have lost his spontaneity. Still another shows aggressive, animalistic behavior--or becomes apathetic, perhaps curling up in the fetal position or sucking, rooting, or grasping as an infant does. Some patients can memorize and recite a long list of numbers, remember events of the day before, and recall many of their childhood experiences--yet they "forget to remember" why they went to the store. When this happens, it's likely that the frontal lobe isn't performing its goal-orienting function as it should. If a patient takes small steps, has trouble initiating a step, or can't seem to find and keep his center of gravity--or if he involuntarily resists or aids an attempt to move his neck, arms, or legs--he doesn't necessarily have Parkinson's disease; he may have a frontal lobe lesion instead. Usually--but not always--the easiest way to find out is to check for a resting tremor.
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PMID:Exploring the enigmas of frontal lobe dysfunction. 82 57

Tremor can be categorized into three general types: resting, action, and intention, Each requires different therapy. Resting tremor is present when the hands are at rest; it disappears with movement. It is characteristic of Parkinson's disease and responds to treatment with L-dopa either alone or in combination with a decarboxylase inhibitor. Action tremor is maximal when the hands are outstretched to the front; it may persist during movement. It is not rare and is often misread as a sign of Parkinson's disease. Propranolol is beneficial. Intention tremor occurs with movement and is characteristic of cerebellar disease. Pharmacologic agents are not helpful. The only known effective treatment is stereotaxic surgery.
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PMID:The shaking patient. Diagnosis and management of tremor. 83 91

We studied a family of Portuguese ancestry from the Azores who suffered a progressive neurologic disease characterized by gait ataxia, features similar to Parkinson's disease in some patients, limitation of eye movements, widespread fasciculations of muscles, loss of reflexes in the lower limbs, followed by nystagmus, mild cerebellar tremor and extensor plantar responses. Two post-mortem examinations revealed loss of neurons and gliosis in the substantia nigra, nuclei pontis (and in the putamen in one case) as well as in the nuclei of the vestibular and other cranial nerves, columns of Clarke and anterior horns, in the spinal cord there were also loss of fibers in the fasciculi gracilis and mild changes in the pyramidal tracts. Comparison of the disease in this family with the findings reported in three families of similar ancestry, previously thought to have different disorders, suggests that they may all represent a single genetic entity with variable expression.
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PMID:Azorean disease of the nervous system. 86 31

We have studied the urinary excretion of 1,4-methylhistamine (1,4-MeHm), 5-hydroxyindole-3-acetic acid (5-HIAA) and homovanillic acid (HVA) in patients with Parkinson's disease, choreiform movements and essential tremor. The effect of amantadine on urinary excretion has been measured in each group of patients as well as the effect of levodopa in patients with Parkinson's disease. In patients with Parkinson's disease, excretion of 1,4-MeHm and HVA was significantly lower than in controls. Patients with choreiform movements had a reduced excretion of HVA but trends toward low levels of 1,4-MeHm and, in patients with Huntington's chorea, elevated excretion of 5-HIAA, were not significant. In patients with essential tremor, urinary excretion of the amine metabolities studied did nof differ significantly from controls. Administration of amantadine to patients with Parkinson's disease was not followed by increased excretion of monoamine metabolites except in those patients who were already receiving anticholinergic drugs. This increase is not significant and there was no effect in other groups of patients. These findings lend no support to the view that amantadine has a general amine-releasing action although there is limited evidence for such an effect in Parkinson's disease. In addition to the expected increase in HVA excretion, administration of levodopa to Parkinsonian patients was followed by significantly reduced excretion of 1,4-MeHm and 5-HIAA. However, if amantadine and levodopa were given together, excretion of 5-HIAA was still reduced, but that of 1,4-MeHm was normal. Levodopa may thus modify the turnover of histamine, which appears to be reduced in Parkinson's disease, and this effect may be modified by amantadine.
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PMID:Urinary monoamine metabolite excretion in disorders of movement. Effects of amantadine and levodopa. 87 21

Disability and progression in Parkinson's disease prior to levodopa treatment was investigated in a random group of 442 patients representing 91 per cent of all known cases with Parkinson's disease in a defined area. Almost half the patients were totally independent, 27 per cent needed help occasionally, and 25 per cent were dependent on other people. Ten per cent of the patients had only unilateral symptoms, 57 per cent had bilateral involvement with mild disability, 20 per cent had a moderately advanced disease, and 13 per cent were severely idsabled. A great variation was found in progression rates. In individual cases, however, the progression rate seemed to be relatively fixed. Concurrent arteriosclerosis was found to worsen the prognosis, whereas the beginning of the disease with tremor and the occurrence of prominent tremor promised a slower progression. Twenty-six patients with only unilateral symptoms 10 years after onset of the disease were found to correspond to postencephalitic patients in age structure, and in such cases a history of preceeding viral infection of the central nervous system was observed on four occasions.
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PMID:Disability and progression in Parkinson's disease. 89 18

Rigidity in Parkinson patients can be easily quantitated by determining net work required to passively flex and extend the forearm through an arc of 100 degrees. Rigidity thus measured can be subdivided into two very distinct types, resting and activated. Resting rigidity, measured while the patient is relaxed, responds to all effective therapeutic agents and correlates closely to degree of clinical improvement. Activated rigidity, measured during voluntary activity, is not relieved by any presently available medical treatment. It remains unchanged at pre-therapy levels even in patients who may temporarily appear to have dramatic improvement in clinical symptomatology. Longitudinal measurements made in hundreds of parkinson patients over intervals ranging from 5 to 15 years show continuing high levels of activated rigidity through the entire period of study. In marked contrast to our wide experience with parkinson patients is a single, well documented case of Wilson's disease who appears to have recovered completely both by clinical examination and by all of our machine measurements. This patient had high levels of extrapyramidal deficit, repeatedly measured over a period of four months when penicillamine therapy was being investigated. He then suddenly reverted to normal and returned to full time employment. High values of resting rigidity activated rigidity, akinesia and resting tremor all reverted to normal and have remained normal for the past 6 years. The implication of this study is that L-dopa and related treatments only mask the symptomatology of Parkinson's disease and are not retarding the underlying pathological process. Penicillamine, on the other hand, probably does relieve the destructive process in Wilson's disease and may in early cases, permanently relieve the extrapyramidal dysfunction.
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PMID:Failure of L-dopa to relieve activated rigidity in Parkinson's disease. 93 Jul 49


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