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)

Four patients with abnormal movements were treated with tiapridal. Very good results were obtained in a case of buccofacial dyskinesia associated with an extrapyramidal syndrome and dementia, and in another patient with middle-of-the-dose dyskinesias induced by L-dopa treatment for Parkinson's disease. No effect was observed, however in a case of beginning of the dose dyskinesias, and the extrapyramidal symptoms increased in severity. A dopadecarboxylase-inhibitor was associated with the L-dopa treatment in these three cases. In the fourth case, there was an increase in the spasms of the medial part of the face.
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PMID:[Cases of abnormal movements]. 3 19

Cerebrospinal fluid gamma-aminobutyric acid (CSF GABA) was analyzed in 151 patients who underwent evaluation for central nervous system disease. CSF GABA was not detected in 19 of these patients, who had no evidence of neurologic disease and who served as controls. GABA was most frequently detected in patients with cerebrovascular disease, and was detected only in Parkinson's syndrome of atherosclerotic origin and dementia of multi-infarct type. CSF GABA was not detected in Alzheimer's disease or Huntington's disease. Patients with grand mal seizures exhibited CSF GABA elevation within 24 hours of the ictus. In patients with multiple sclerosis GABA detection was related to the presence or exacerbation of spinal cord lesions. Further study is necessary to evaluate the significance of elevated CSF GABA in central nervous system disease.
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PMID:Cerebrospinal fluid gamma-aminobutyric acid in neurologic disease. 13 99

The habituation index is a quantitative expression of the ability of the orbicularis oculi (blink reflex) to adapt to a series of electrical stimuli applied to the supraorbital region. This parameter has been studied in a group of normal control subjects, and the results compared with those in cases of idiopathic and drug-induced Parkinsonism, states of dementia, and dyskinesias such as Huntington's chorea and senile chorea. Patients with Huntington's chorea showed a tendency for the reflex to habituate readily in contrast to patients with dementia caused by cortical atrophy and those with Parkinson's disease. Younger patients with Huntington's chorea had indices within the normal range. It seems unlikely that this test will prove of value in the detection of clinically unaffected relatives. Where dementia was associated with a reversible intracranial lesion, the habituation index was studied before and after treatment. Failure of habituation in this condition appears to be due to the release of a primitive protective reflex.
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PMID:Habituation of the orbicularis oculi reflex in dementia and dyskinetic states. 15 Nov 27

A group of diseases of the brain characterized by dementia have been discussed. The pathologic features of each were described and illustrated. It seems that, in summary, several points merit emphasis. First of all, as more people survive to the seventh, eighth, and ninth decades, the most common dementia, senile Alzheimer's disease, will become a more significant public health problem. Second, while at the present time there is no successful therapy available, there are some glimmerings of hope on the horizon. The discovery of the agent of Creutzfeldt-Jakob disease seems to have placed us on the fringe of a whole new series of advances. A novel type of disease agent awaits characterization and definition, and there are hints that similar agents could be responsible for the development of the degenerative diseases, perhaps in conjunction with environmental toxins and in the medium of a permissive genetic background. In the case of Huntington's chorea, it seems reasonable that a pharmacologic agent could be found to control the symptoms such as L-dopa therapy has done for patients with Parkinson's disease. It may develop, however, that such an agent will control the choreiform movements but will not influence the dementing condition.
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PMID:Pathology of dementia. 16 30

Large numbers of Lewy bodies in the substantia nigra were found in a case of Alzheimer's disease. Parkinsonian symptoms were not recognized. The patient appears to be an example of an association recognized by Woodard but not yet understood. The case is discussed in the context of reported relationships between Parkinson's disease or "Lewy body disease" and dementia, on the one hand, and reports linking various forms of psychoses with an unusually high incidence of Lewy bodies, on the other.
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PMID:Lewy bodies in the presence of Alzheimer's disease. 21 17

Five cases of age range 62-72 years with progressive dementia and muscular rigidity are reported and discussed from the clinicopathologic point of view. The neuropathology of these cases was characterized by the widespread occurrence of Lewy bodies (LB) in the CNS as well as the presence of senile changes. The presence of numerous LB in the cerebral cortex and basal ganglia was especially characteristic, although their distribution pattern in the diencephalon and brain stem was identical to that found in paralysis agitans. On the other hand, the presence of senile changes in the cerebral cortex was almost identical to the neuropathology of senile dementia or Alzheimer's disease. Nosologically, the present cases may represent either a combination of atypical paralysis agitans with senile dementia and Alzheimer's disease, or a new disease.
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PMID:Dementia-Parkinsonism syndrome with numerous Lewy bodies and senile plaques in cerebral cortex. 22 31

An inquiry was made into the physical and behavioural problems presented by patients admitted to hospital because of dementia. 81 patients were studied over a period of 3 years, and a comparison was made between the 38 with idiopathic (Alzheimer's) dementia, and the others, most of whom suffered from focal cerebral arteriosclerosis or Parkinson's disease with dementia. The average age was between 70 and 80 years, and the hospital stay averaged 18-28 months. Nursing difficulties ranged from immobility of the patients on the one hand to wandering on the other, especially in the Alzheimer's group. Behaviour disturbances, shouting, incontinence and degenerate habits were found in a high proportion and the incidence of fractures reached 15%. Vascular incidents as complications or causes of death were relatively uncommon; in those who died, the cause was usually infection. The mainstays of treatment were tranquillising drugs, used only when necessary, and in minimal quantities, simple occupational activity, and an awareness by the staff of the high morbidity to which these patients were prone.
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PMID:The physical and behavioural complex of dementia. 40 46

BRomocriptine (15-75 mg per day) alone or with L-dopa was studied during five to 29 months on 44 patients with Parkinson's disease. Used as sole therapeutic agent, it was found excellent in 12 patients who had never received regular L-dopa treatment either because it was never attempted or because of intolerance from the outset. Its anti-Parkinsonism activity was comparable with L-dopa. The gain was stable in the long term until this report. The side effects of L-dopa were not seen after bromocriptine. In cases where L-dopa had ceased to be active, bromocriptine produced a further improvement if mental deterioration was not associated. In very advanced forms of Parkinson's disease with associated dementia, bromocriptine did not produce durable results. Bromocriptine did not improve the "on-off" effects but reduced a number of the side effects of L-dopa, in particular cardiac, painful contractions, and dyskinesia without "on-off" effects.
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PMID:Long-term treatment of Parkinson's disease with bromocriptine. 42 61

Recent studies suggest that levodopa treatment reduces the excess mortality due to Parkinson's disease, found to be three times that expected in the general population. This will affect the equilibrium state of the epidemiology of Parkinson's disease. The predicted increase in prevalence of Parkinson's disease was calculated according to two mortality patterns, one the same as expected in the general population and the other 1.5 times that expected; the proportional increase in prevalence is 1.8 and 1.4, respectively. The predicted increase in the duration of the disease if 6.3 or 3.2 years. As a consequence, there will be an increase of patients with long-term levodopa treatment difficulties, and with Parkinson's disease symptoms not treatable with levodopa, e.g. dementia. This seriously warrants the research of new approaches in the treatment of Parkinson's disease.
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PMID:Changing epidemiology of Parkinson's disease: predicted effects of levodopa treatment. 45 43

Recent studies have shown a defect in the cholinergic system of the cerebral cortex of patients suffering from nonvascular senile dementia. This observation suggests the possibility of instituting some kind of replacement therapy and trial have been carried out. At this juncture it seem pertinent to ask what lessons can we learn from Parkinson's disease, what is the evidence for a biochemical defect, is this defect relevant and can it be remedied? These questions are considered in turn and suggestions are made about the likely difficulties to be overcome in a search for a treatment of dementia.
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PMID:Will drugs help patients with Alzheimer's disease? 46 80


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