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  • 1
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 42 (1978), S. 151-157 
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Bromocriptine was used as a treatment for Parkinson's disease in 15 patients for 20 weeks. Immunoreactive plasma lutrophin (LH), follitrophin (FSH), prolactin, and somatotrophin (GH, growth hormone) concentrations were analysed before and during the treatment. Plasma prolactin levels were very markedly reduced during treatment. Plasma lutrophin levels were increased statistically significantly in female patients, but not in male patients. No changes were noticed in follitrophin levels, but plasma somatotrophin levels were reduced during treatment. No correlations were found between the degree of clinical response and changes in plasma gonadotrophin and somatotrophin. This suggests that the effects of bromocriptine on extrapyramidal and neuroendocrine dopaminergic neurons are unrelated. We suggest careful and frequent controls of neuroendocrine secretion patterns in patients with Parkinson's disease who are treated with high doses of dopamine receptor stimulators, since the responses of some pituitary hormones to bromocriptine are very marked.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1435-1463
    Keywords: Alzheimer's disease ; multi-infarct dementia ; combined dementia ; choline acetyltransferase ; post-mortem brain studies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Brain choline acetyltransferase (ChAT) activity was determined in 43 patients with Alzheimer's disease (AD), 14 with multi-infarct dementia (MID), and 15 with combined dementia (CD) and in 53 age-matched controls. The activity of ChAT declined in the hippocampus, temporal and frontal cortex in patients with AD and CD compared to the controls. In the AD group the reduced activity of ChAT in all brain areas was associated with a greater number of cortical neurofibrillary tangles. The degree of dementia had a negative correlation with the activity of ChAT in the frontal cortex in both AD and CD patients. The activity of ChAT in the temporal cortex of CD patients was negatively associated with the cortical tangle counts. In contrast, the activity of ChAT and MID patients was not essentially different from that of the controls. Neither did the various clinical and neuropathological variables show any significant correlation with ChAT activity in MID patients. Thus, in this study the reduction in the activity of ChAT seems to be associated with Alzheimer-type pathology but not with dementia due to vascular changes.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 51 (1981), S. 1-1 
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 51 (1981), S. 97-106 
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Striatal dopamine receptors were studied in 44 patients with Parkinson disease by the radioligand-binding technique using3H-spiroperidol. The specific binding of3H-spiroperidol was either significantly increased or reduced in the caudate nucleus and putamen of parkinsonian patients without levodopa therapy. Scatchard analysis showed that there were corresponding changes in the receptor number, but no significant changes in the mean dissociation constant. The increased binding of3H-spiroperidol in the basal ganglia was also found in parkinsonian patients suffering from psychotic episodes and treated with neuroleptic drugs. Normal and low binding of3H-spiroperidol was found in patients treated with levodopa. Clinically, the patients with low binding were more disabled and had lost the beneficial response to levodopa. Thus in Parkinson disease in some patients a denervation supersensitivity seemed to develop and in some others a loss of postsynaptic dopamine receptor sites in the neostriaturn. The latter alteration may contribute to the decreased response of parkinsonian patients to chronic levodopa therapy.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 34 (1973), S. 145-151 
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Blood levels of growth hormone, insulin and glucose were studied in 63 patients before and after intravenous levodopa (1.5 mg/kg), oral levodopa (0.5 g and 1.0 g) and amantadine (100 mg). A significant increase of growth hormone concentrations was found after intravenous and oral 1.0 g doses. No significant differences were found in insulin and glucose concentrations.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 25 (1963), S. 310-324 
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 43 (1978), S. 253-262 
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of L-deprenyl were investigated in 47 parkinsonian patients under chronic levodopa treatment with our without on-off phenomena. During a 1 to 3 months' treatment 5–10 mg of L-deprenyl caused a significant reduction in on-off disabilities in 23 out of 34 patients (68%). The improvement was only moderate (38%) or minimal (30%). All patterns of akinetic on-off disabilities showed improvement. Peak-dose dyskinesias were aggravated in 20 patients. The addition of L-deprenyl to levodopa treatment caused a further significant improvement in parkinsonian disability. Responses to L-deprenyl were similar in patients treated with levodopa alone and in those treated with levodopa combined with a decarboxylase inhibitor. L-deprenyl induced a significant increase in the urinary excretion of dopamine but not in that of VMA or 5-HIAA. Concentrations of HVA and 5-HIAA in the CSF remained unchanged during L-deprenyl treatment. It was concluded that L-deprenyl seems to provide a valuable adjuvant to levodopa in patients with on-off disabilities.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 51 (1981), S. 135-148 
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Among the white races, the prevalence rates of Parkinson's disease range from 66 to 187 per 100,000 population, through without any obvious geographical pattern. A similar variation is found in the annual incidence rates with estimates from 5 to 24 per 100,000 population. The black races may be partially protected against the disease. Both sexes are probably equally affected by the disease. Parkinson's disease usually begins after the age of 50 years, and the risk of the disease steeply rises with advancing age. Parkinson's disease is often omitted in death certificates; mortality rates with Parkinson's disease as an underlying cause of death vary from 0.5 to 3.8 per 100,000. Levodopa treatment, by reducing the excess mortality accompanying the natural course of Parkinson's disease, may increase the number of patients living with this disease in the near future. Postencephalitic Parkinson's disease, developing as a sequel to lethargic encephalitis and accounting for some two thirds of parkinsonian cases shortly after the epidemic, has probably been a transient phase in the epidemiology of Parkinson's disease and is now disappearing. Data from epidemiological investigations have advanced our understanding of the cause of Parkinson's disease only to a small extent. No other characteristic than race has been found to influence the susceptibility to the disease. The environmental risks for Parkinson's disease have not been unequivocally demonstrated. Highly conflicting information is available as to the contribution of heredity to the pathogenesis of Parkinson's disease. Seroepidemiological investigations have shown an increased antibody response against herpes simplex virus in parkinsonian patients, but attempts to detect herpes virus specific products or DNA sequences in the brain material have been unsuccessful. Further epidemiological research on Parkinson's discase, with strict diagnostic criteria, is needed to clarify the racial occurrence, to establish the true role of heredity, and to uncover possible enviornmental risks.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 51 (1981), S. 161-174 
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Long-term follow-up of parkinsonian patients has shown that although levodopa treatment significantly improves the parkinsonian symptoms and the quality of life of parkinsonian patients for several years, various distressing difficulties arise during chronic levodopa treatment, such as the loss of benefit, dyskinesias, on-off phenomena, postural instability and dementia. Clinical, neuropsychological, mortality and post-mortem brain studies indicate that levodopa as a replacement therapy does not modify the progression of the underlying pathology and the natural course of the disease. It seems that levodopa has only a limited period of optimal usefulness in the treatment of Parkinson's disease. However, at present there is no better or more potent therapeutic agent available than levodopa and it is still the primary treatment of Parkinson's disease. It would be reasonable not to begin levodopa treatment in patients with mild symptoms but to withold levodopa until the severity of symptoms really makes its use necessary. Thus it is possible to get the maximal long functional benefit. Post-mortem brain studies have shown that in Parkinson's disease there is not only a progressive loss of dopaminergic substantia nigra neurons but there are also significant changes in the striatal dopamine receptors. In some patients a denervation supersensitivity seems to develop and in some others a loss of dopamine receptors in the striatum. However, in advanced parkinsonian patients with a deteriorating response to levodopa, there seem to be still enough dopamine receptors in the striatum for drugs stimulating the dopamine receptors directly to improve the parkinsonian disability. Indeed, recent evidence indicates that dopaminergic agonists, such as bromocriptine, seem to be a significant and valuable adjuvant therapy to levodopa in parkinsonian patients with a deteriorating response and/or the on-off phenomena. Although bromocriptine is not completely satisfactory, it is a significant opening to a new mode of treatment. In the future it will be very important to develop more potent and selective dopaminergic agonists affecting only those striatal receptors which are mainly responsible for the parkinsonian symptoms. Then a better therapeutic response is likely to occur and many central side effects can be avoided. Current difficulties in the management of Parkinson's disease greatly depend on the fact that we are dealing with a symptomatic therapy. It is hoped that future research will soon lead to a discovery of the primary cause and consequently to a causal therapy of Parkinson's disease.
    Type of Medium: Electronic Resource
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