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)

The effects of carbidopa combined with levodopa (carbidopa/levodopa) and levodopa alone on the cardiovascular system of patients with Parkinson's disease were evaluated. Thirty-eight patients who had been on stable doses of levodopa underwent a complete cardiac examination, including measurement of recumbent and erect blood pressure and 24 hour ambulatory electrocardiographic monitoring. Patients were classified with respect to the presence or absence of clinically significant heart disease and ventricular arrhythmias. Nineteen of the 38 patients (50 percent) had heart disease, and 12 (32 percent) had significant ventricular arrhythmias. Eleven of the 12 with arrhythmias had underlying heart disease. The incidence of arrhythmias did not correlate with the dose of levodopa. The patients were subsequently randomly assigned to treatment groups receiving either carbidopa/levodopa or levodopa alone. There was no significant difference in the severity of ventricular arrhythmias or in the incidence of orthostatic hypotension in the group assigned to carbidopa/levodopa compared with the group receiving levodopa.
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PMID:Comparison of dopa decarboxylase inhibitor (carbidopa) combined with levodopa and levodopa alone on the cardiovascular system of patients with parkinson's disease. 5 31

Simultaneous recording was performed from pairs of motor units either in a small intrinsic hand muscle (first dorsal interosseus, 6 subjects, 37 records) or in two synergistic calf muscles (gastrocnemius and soleus, 6 subjects, 50 records). The two motor units were recorded by means of two electrodes inserted into the muscle during stationary isometric contractions of different strengths. Cross-correlograms were calculated in two ways: (1) between spike trains of two motor units; (2) between either spike train and the peaks of the tremor record. The cross-correlation between pairs of motor units showed a consistent tendency to synchronization in the hand as well as in the calf muscles. This synchronization was higher than could be expected from the random activity of asynchronously firing motor units. The amount of synchronization was correlated with the amplitude of physiological tremor: the stronger the tremor, the higher the synchronization coefficient. The cross-correlation between a spike train and the peaks of the tremor records showed a higher probability of unit firing 30-60 msec prior to the tremor beats. It is concluded that the tremor force produced by one muscle or a pair of synergistic muscles is the result of the synchronized activity of motor units. This hypothesis is supported by some characteristic changes in the amplitudes and rates of tremor in Parkinson's disease and myopathies. In these diseases the pathological changes in tremor rates simply reflect underlying changes of the motoneuronal firing rates.
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PMID:Correlation between the dischanges of two simultaneously recorded motor units and physiological tremor. 5 52

Fluctuations in performance in patients with Parkinson's disease on chronic levodopa therapy (the "on-off" effect) are due to several factors. The increasing severity during treatment of early morning akinesia, "freezing" episodes, and end-of-dose deterioration are probably due to progression of the underlying disease. Peak-dose dyskinesia and peak-dose akinesia are due to levodopa over dosage. "Yo-yo-ing", which is the severest form of such fluctuation in mobility and dyskinesias, may represent the sum of these disorders.
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PMID:"On-off" effects in patients with Parkinson's disease on chronic levodopa therapy. 5 99

A combination of levodopa and the extracerebrally acting decarboxylase inhibitor benserazide (ratio 4:1) (Madopar), was compared with levodopa alone in a controlled double-blind clinical multicenter trial on 94 patients with Parkinson's disease. During 4 months of therapy levodopa + benserazide proved superior to levodopa on several accounts. Nausea and vomiting occurred with statistically significant less severity and frequency. Clinical improvement expressed through improvement in Webster rating occurred sooner and was all together greater. The treatment schedules did not differ with regard to other side effects, in particular involuntary movements and reduction in supine blood pressure. Neither treatment seemed to influence liver function, renal function and hematological parameters.
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PMID:Levodopa alone and in combination with a peripheral decarboxylase inhibitor benserazide (Madopar) in the treatment of Parkinson's disease: A controlled clinical trial. 5 27

Parkinson's disease is characterised by an imbalance between acetylcholine and dopamine which probably results from the degeneration of a dopaminergic nigrostriatal pathway. A new hypothesis is proposed to explain the development of this imbalance. Applying the concept that degeneration of nerve-fibres in the central nervous system can lead to collateral sprouting of uninjured fibres, it is suggested that the death of dopaminergic nigrostriatal neurons results in sprouting of axons of cholinergic interneurons in the caudate nucleus. This overgrowth could result in the cholinergic innervation of neuronal membranes vacated by degenerated dopaminergic terminals. Thus, the apparent changes in the activity of dopaminergic and cholinergic systems can be accounted for by faulty regeneration in the central nervous system.
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PMID:Dopamine acetylcholine imbalance in Parkinson's disease. Possible regenerative overgrowth of cholinergic axon terminals. 5 38

Amyotrophic lateral sclerosis (ALS) and Parkinson disease (PD) are known to occur simultaneously among some Chamorro inhabitants of Guam and other Mariana Islands (Stanhope et al., 1972). Outside of the Western Pacific Islands, the concurrence of ALS and PD seems to be rare. However, it has been observed to occur with sufficient frequency to suggest some causal association. The following is a report of a patient suffering from ALS whose family history included PD in several of the immediate relatives.
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PMID:A family with amyotrophic lateral sclerosis and Parkinsonism. 5 79

The CSF proteins have previously been very little investigated in the cerebellar syndrome of chronic alcoholism and in essential tremor. Such studies have been carried out more thoroughly by electrophoretic methods in Parkinson's disease but generally with normal results. In the present investigation the CSF proteins were examined by isoelectric focusing and quantitative paper electrophoresis in 10 patients with the cerebellar syndrome of chronic alcoholsm, 12 patients with Parkinson's disease and 16 subjects with essential tremor. Abnormal CSF proteins of very similar appearance were found on isoelectric focusing in the acidic pH interval 5.6-5.8 in 80% of the patients with the cerebellar syndrome of chronic alcoholism. In Parkinson's disease the most common aberration was evidence of nonspecific blood-CSF-barrier damage which occurred in half of the patients. In only 17% of these cases did other alterations appear, situated in the pH range alkaline to pH 5.8. Abnormal CSF proteins were found in 94% of the patients with essential tremor. The aberrant proteins appeared in both the acidic and alkaline pH regions, most frequently with anisoelectric point at pH 5.9, 7.2 and 9.3. There was a considerably higher frequency of CSF protein abnormalities in different pH ranges in patients with tremor of more pronounced degree as compared to those with only mild symptoms. The electrophoretic examinations failed to show any conclusive alterations. Barrier-damage patterns of mild or moderate degree or slightly increased levels of CSF beta1-globulin were occasionally found in all 3 diseases. The results indicate that isoelectric focusing of the CSF proteins may be of diagnostic value in the cerebellar syndrome of chronic alcoholism and in essential tremor but does not reveal any characteristic abnormalities in Parkinson's disease.
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PMID:Isoelectric focusing and electrophoresis of the CSF proteins in tremor of different origins. 6 43

The patient with Parkinson' disease on chronic levodopa therapy, like the diabetic on insulin, is dependent on the drug. Like the diabetic, the patients with Parkinson's disease may run into problems during long-term treatment. Two have emerged as frequent and serious, an insidious and progressive loss of benefit and the appearance of progessively more severe fluctuations in disability. It is concluded that progression of the underlying pathology of the disease is probably responsible. Discovery of the exact causes for loss of benefit may provide a rational basis for new therapy.
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PMID:Success and problems of long-term levodopa therapy in Parkinson's disease. 6 68

Clinical EEG evaluation and power spectral analysis were performed on 12 parkinsonian patients before and during L-DOPA treatment. The EEG evaluation did not disclose any significant effects of L-DOPA treatment. Spectral analysis disclosed normal interlobar and interhemispheric power differences and an increase in delta and slow-theta power in the right temporal as compared to the right occipital lobe before L-DOPA treatment was initiated. L-DOPA treatment significantly increased alpha power in both occipital lobes, decreased theta power in the right temporal lobe, accentuated power differences in the theta and alpha bands between temporal and occipital lobes and attenuated beta power differences in those areas. This work is intended as a pilot study in the quantitative EEG evaluation of Parkinson's disease and L-DOPA treatment.
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PMID:EEG power spectral changes secondary to L-DOPA treatment in parkinsonian patients: a pilot study. 6 67

In a double-blind crossover trial, (-)-deprenyl, a fast-acting selective monoamine-oxidase-B inhibitor without a "cheese effect", was given to 41 patients with idiopathic Parkinson's disease who were receiving maximum tolerated doses of levodopa either alone or combined with carbidopa ("Sinemet"). In a dose of 10 mg, daily or on alternate days, (-)-deprenyl prolonged the therapeutic effect of levodopa and was effective in mild "on-off" disabilities with end-of-dose akinesia; the majority of patients with nocturnal and early-morning akinesia also improved. No statistically significant improvement occurred in diurnal akinesia, and there was no improvement in patients with severe on-off disabilities with freezing and rapid oscillations ("yo-yo" effect). Levodopa-induced dyskinesias were aggravated in 14 patients. In 5 previously untreated patients, (-)-deprenyl alone gave no benefit, but when it was used with levodopa and carbidopa a mean dosage reduction of 200 mg levodopa daily was possible. Depression, present in 15 patients, was unchanged. (-)-Deprenyl in combination with smaller total daily doses of levodopa and a peripheral decarboxylase inhibitor may prove useful in reducing the frequency and severity of some types of on-off effect with overall benefit comparable to that obtained with larger doses of levodopa.
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PMID:Deprenyl in Parkinson's disease. 7 2


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