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Levodopa combined with carbidopa is still the most effective treatment for symptoms of Parkinson's disease. Dopamine agonists, the next most effective class of drugs, can be used alone before the introduction of levodopa or as an adjunct to levodopa.Addition of a peripherally-acting COMT inhibitor or an MAO-B inhibitor to levodopa can reduce motor fluctuations in patients with advanced disease.Amantadine may have mild symptomatic benefit and can decrease levodopa-induced dyskinesias.Anticholinergics are rarely used because of their adverse effects, but can be a useful addition to levodopa for control of tremor and drooling.Subcutaneous apomorphine should be available for rescue use in patients with 'off' episodes. Deep brain stimulation is an option for patients with levodopa-induced motor complications and relatively intact cognition.
sinemet starting dose
The nature of sleep is one of the major sources of dissatisfaction with the quality of life among patients with Parkinson's disease (PD). Difficult sleep maintenance (light and fragmented sleep) and difficulties with sleep initiation are the earliest and most frequent sleep disorders observed in these patients. Sleep disorders are also common in the normal elderly population, suggesting that normal aging may play a role in the etiology of sleep disorders in PD. Factor et al. examined the frequency of various sleep disorders in PD and compared them to those of normal elderly subjects. Sleep fragmentation and spontaneous daytime dozing occurred much more frequently in PD patients than in controls. Sleep fragmentation in PD may be due to an increased skeletal muscle activity, disturbed breathing and REM/non-REM variations of the dopaminergic receptor sensitivity. In parkinsonian patients who developed motor fluctuations (on-off phenomenon, wearing-off) during the day, other common sleep-related motor complaints including nocturnal akinesia, dystonia and painful cramps are observed. In a double-blind cross-over study, we compared the efficacy of a single dose of a chronic release formulation of levodopa/carbidopa (Sinemet CR) with that of a placebo in improving sleep-related motor disturbances in a group of 40 fluctuating PD patients. Sinemet CR significantly improved nocturnal akinesia and increased the hours of sleep in this group of patients. Initiation and maintenance of sleep are problems that may not be solved with antiparkinsonian treatment.
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We examined and videotaped all homozygous carriers of the DYT16 gene.
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Levodopa combined with carbidopa (Sinemet) remains the most effective approach to the symptomatic relief of Parkinson's disease. Over time, however, an increasing number of parkinsonian patients evidence motor response complications, notably abnormal involuntary movements and motor fluctuations. Clinical pharmacologic studies suggest that these phenomena may arise as a consequence of factors reflecting both natural disease progression and levodopa toxicity. Simple wearing-off responses appear primarily related to advancing degenerative changes afflicting the dopamine system. The appearance of peak-dose dyskinesias and complex, random motor fluctuations of the on-off type, on the other hand, may signal secondary postjunctional changes arising as a consequence of chronic intermittent excitation of postsynaptic dopamine receptors that are normally tonically stimulated. Therapeutically, prompt correction of wearing-off fluctuations can ordinarily be achieved by measures that deliver dopaminomimetics continuously to the central nervous system. In contrast, fluctuations of the on-off type initially persist despite stable circulating levodopa levels. With continuous levodopa treatment, however, the threshold for dyskinesias begins to rise and the dose-response relation shifts to the right; clinically, the severity of both dyskinesias and on-off fluctuations tends to diminish. It is thus tempting to speculate that the early and continuing treatment of Parkinson's disease with compounds providing a relatively constant level of central dopamine stimulation will preclude wearing-off phenomena and mitigate on-off fluctuations and severe dyskinesias.
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Dyskinesias associated with dopaminergic treatment in idiopathic Parkinson's disease (PD) can be indistinguishable from those arising spontaneously in other conditions involving degeneration of, or damage to, the basal ganglia. However, those due to levodopa treatment of PD disappear on cessation of therapy. We report a patient with a clinical diagnosis of PD who, on levodopa treatment, developed hemiballism and chorea that were originally thought to be drug induced. However, the dyskinesias persisted despite stopping levodopa. Postmortem analysis showed a multisystem degeneration.
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The influence of meal ingestion time on rate and extent of oral levodopa absorption was evaluated in a group of 17 patients, after administration of their usual second daily dose of levodopa plus carbidopa (Sinemet 10:1) or benserazide (Madopar 4:1). Standard meals were consumed by the patients after they had fasted 15-17 h, on one occasion 30 min before ingestion of the levodopa "study dose" and, at another time, 2 h after ingestion of the same dose. This study dose, ranging from 50 to 250 mg levodopa, was given to the patients at 11 a.m., 4 h after their first morning dose. Time to peak plasma levodopa concentration increased threefold (from 45 +/- 23 to 134 +/- 76 min, p less than 0.001), when levodopa was administered after meals. Area under the 6-h plasma concentration-time curve for levodopa was decreased in 10 subjects, unchanged in three and higher in four after ingestion of meals, the latter finding probably resulting from an erratic absorption even at fasting. On the whole, levodopa absorption proved significantly lower (p less than 0.01), on the average 15%. Similarly, peak plasma levodopa concentrations were lower in 12 patients, unchanged in two, and higher in three, with an overall significant decrease (p less than 0.001) of 30% on the average. The data confirm the importance of meal ingestion time in relation to levodopa dose as a determinant of drug absorption.
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A recent clinical trial of controlled-release carbidopa/levodopa preparation afforded us the opportunity to examine the effects of chronically increasing circulating 3-O-methyldopa (OMD) levels on the clinical response to levodopa. In patients taking standard Sinemet, both mean plasma OMD levels and the area under the plasma concentration-versus-time curve (AUC) obtained during 8-hour periods of blood sampling correlated highly with the total daily intake of levodopa. In patients taking the controlled-release formulation, the mean daily intake of levodopa was doubled. This, in turn, led to a doubling of the mean OMD level and its AUC, whereas the AUC for levodopa was unchanged. Despite the increase in circulating OMD there was no reduction in mobility in either the "on" or "off" conditions. Thus, doubling plasma OMD levels did not seem to interfere with brain uptake of levodopa sufficiently to cause a deterioration in its therapeutic efficacy in these patients.
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The objective was to investigate the neuroprotective role of Beta vulgaris in Parkinson's disease (PD).
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To compare the costs of pharmacotherapy in patients with Parkinson's disease before and after converting from standard Sinemet to extended-release Sinemet CR.
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Levodopa/carbidopa intestinal gel (LCIG) infusion is nowadays becoming an established therapeutic option for advanced Parkinson's disease (PD) patients with fluctuating symptoms unresponsive to conventional oral treatment. As the implementation of LCIG therapy is increasing, there is a need for safety and efficacy data from current clinical practice.
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Contrary to a previous report, pretreatment of normal men with carbidopa plus L-dopa (Sinemet 25/250) markedly inhibited the PRL response to TRH, a stimulus that acts directly on the pituitary. Thus, the results of carbidopa/L-dopa testing cannot be used to determine whether agents that stimulate PRL secretion act on the pituitary or at a higher central nervous system level.
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New concepts about the pathogenesis and pathophysiology of Parkinson's disease have emerged. For these concepts to be useful, they must be understood, and for them to be applied, the psychology of the patient and the patient's family must be understood. The initial consultation is crucial in establishing a successful relationship between a patient, family, and physician. This consultation is analyzed and ways of avoiding errors and misconceptions delineated. Emphasis is placed on imaginitive questioning using the format of the ADL portion of the UPDRS in establishing the diagnosis and following treatment. The rational for starting treatment with selegiline at this time is discussed in the context of the role that increased MAO-B activity plays in the progression of Parkinson's disease. After making the diagnosis and starting treatment with selegiline, deciding when to start levodopa is the next crucial decision. Often as important as deciding when to start levodopa is overcoming the resistance of the patient to accept this treatment. The next crucial decision occurs after the patient develops response fluctuations on levodopa. A format for assessing the fluctuations is presented, and the merits of different treatments, including selegiline, dopamine agonists (bromocriptine and pergolide), and sustained-release or controlled-release levodopa preparations (Sinemet CR), discussed. The management of patients with depression, sleep problems, and advanced disease including postural instability and mental changes are reviewed.
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Plasma prolactin (PRL) levels modifications after acute administration of L-dopa, L-dopa plus carbidopa and L-dopa plus benserazide were studied in parkinsonian patients. PRL increase after benserazide was compared with PRL response after carbidopa at the same dosage in untreated parkinsonian patients. A further study of the hyperprolactinemic effect of benserazide was performed in vitro on isolated and dispersed rat pituitary cells. The data gathered indicate that benserazide-induced hyperprolactinemia in parkinsonian patients could be due to a direct effect of the drug at the hypothalamic level and consequently to an inhibition of dopamine decarboxylation in the tuberoinfundibular dopaminergic system. It is not possible to exclude, however, that benserazide could exert its biological activity through the production of active metabolites in vivo.
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Infusion of levodopa/carbidopa intestinal gel (Duodopa ; Abbott) was introduced in Sweden in 1991 as an experimental treatment in advanced Parkinson's disease and obtained EU approval in 2004. There is compelling evidence for short-term use of this treatment; however, long-term data are scarce.
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Fifty-one patients were enrolled in a double-blind, parallel group, multicentre study conducted to assess short-term efficacy and tolerance of bromocriptine (Parlodel) or L-DOPA/carbidopa (Sinemet) in patients never treated with amantadine, ergot alkaloids or L-DOPA-based drugs. An attempt to use the lowest effective dose was made. The responder rate for each group was approximately 78%; the mean daily dose for responders was 22.5 mg of bromocriptine or 250 mg of L-DOPA/carbidopa. The overall clinical improvement in each group was 62% (bromocriptine) and 55% (L-DOPA/carbidopa) for neurological assessment and 36% (bromocriptine) and 31% (L-DOPA/carbidopa) for functional disability. Comparison between groups did not show any significant difference for both neurological and disability assessments. The most frequent side effect was nausea (L-DOPA, N = 3; bromocriptine, N = 6).
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In 68 younger de novo patients with the hypokinetic-rigid type of PD the action of bromocriptine, Sinemet, a combination of these drugs, and orphenadrine with additional bromocriptine or Sinemet medication was investigated over at least a 6-year period. The favorable reaction on Sinemet medication was complicated by the occurrence of dyskinesias in the majority of cases as contrasted with the bromocriptine group. Dyskinesias were mild and not prominent in the combined group. In the sixth year, it appeared necessary to increase the dosage in the first three groups. Temporary complete replacement after 5 years of Sinemet by bromocriptine caused a clinical deterioration, whereas the dyskinesias did not (completely) disappear. Both drugs markedly improved the hypokinesia in the orphenadrine group. The results in the old-age category (60 patients) without high vascular risk were comparable with those of the young patients. The same applied for those PD patients with high vascular risk, in whom the cerebral circulation could be restored. The final conclusion of this study can be formulated as follows: Primary multitherapy with low dosage bromocriptine and a levodopa preparation may be the therapy of choice. In case of high vascular risk, improvement of the cerebral circulation may be as important as treatment with anti-parkinsonian drugs.
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100 patients with motor fluctuations who had undergone an initial 6-month course of Sinemet therapy, followed by a 6-month course of Sinemet CR.
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The report is based on the observation of 39 patients with parkinsonian syndromes treated with L-DOPA with inhibitor, including 30 patients treated during 2-6 years. It was found that treatment with L-DOPA with the inhibitor gave good or very good results in most patients with these syndromes with a relatively good drug tolerance during the first three months. With passing time the effect of the drug on the manifestations of the disease decreases and the tolerance becomes aver worse. The results of the treatment are worse although the applied daily dose is increased by a metan value of 50%. AT the same time the frequency of such complications as hyperkineses, anxiety and depression labyrinthine-cerebellar signs increases. Urinary passage disturbances and mental degradation develop and their temporal association with L-DOPA treatment is unquestionable, while a cause-and-effect correlation seems likely. In the conclusion the author suggests the need for a careful consideration of each decision of treatment with L-DOPA, and the possibility of improving the results of parkinsonism treatment is seen in the production of new optimal forms of he already present drugs, monitoring blood drug levels, and practical utilization of the synergism between the group of drugs stimulating the dopaminergic system and the group of drugs inhibiting the acetylcholinergic system.
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We converted 158 Parkinson's disease (PD) patients on stable doses of standard carbidopa/levodopa (Std-L) to controlled-release carbidopa/levodopa (L-CR). Of the 141 patients who completed the study, 103 (73%) preferred L-CR, 26 (18.5%) preferred Std-L, and 12 (8.5%) had no preference. One hundred fourteen patients elected to continue L-CR, and we performed the primary data analysis on this group. Following conversion to L-CR, patients reported an increase in length of benefit from each dose and an increased "kick-in" time. There was a decrease in the total number of doses, "off" periods, sleep interruptions per night, dose failures, and sleep disturbances. Conversion to L-CR resulted in a significant increase in total levodopa dose. There was no significant change in the dyskinesias. However, early-morning dystonia resolved in eight of 14 patients. Our findings suggest that L-CR is particularly effective in decreasing motor fluctuations, reducing nocturnal problems, and minimizing levodopa dose failures in PD.
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Seventeen patients with advanced Parkinson's disease who had fluctuations in motor performance while taking standard Sinemet (STD) 25/100 underwent daylong pharmacokinetic and clinical observation studies while taking both STD and Sinemet CR, a new controlled-release formulation containing 50 mg carbidopa and 200 mg levodopa. During treatment with Sinemet CR, there was an increase in the interdose interval, a reduction in the number of medication doses taken each day, an increase in total "on" time, and a reduction in the number of "off" episodes. Total daily levodopa intake was greater with Sinemet CR, although the bioavailability of levodopa and carbidopa from the two preparations was equivalent. The variability in plasma levodopa levels was significantly less with Sinemet CR. The slower release of drug from Sinemet CR was reflected in a prolongation of the Tmax for levodopa and a prolongation of the interval from Tmax to the succeeding trough levodopa level. Clinically, peak antiparkinsonian effect occurred later and lasted longer with the CR preparation.
PPN discharge characteristics may prove useful in the electrophysiological identification of PPN during DBS implantation surgery.