sinemet dosage forms
The multiple-dose (200 mg levodopa t.i.d.) pharmacokinetic profile of two controlled-release products of levodopa (Madopar HBS and Sinemet CR) was compared to conventional Madopar capsules in 18 healthy volunteers in a cross-over, randomized design. A pronounced controlled-release profile of the Madopar HBS and Sinemet CR product was demonstrated compared to conventional Madopar capsules with a significant (p < 0.001) decrease (-40 and -55%) in Cmax and a significant (p < 0.001) increase (+237 and +256%) in morning Cmin for the 200 mg t.i.d. dosage schedule. Almost equivalent bioavailability (85-90%) of levodopa was demonstrated for the controlled-release formulations relative to that of conventional Madopar capsules. The Madopar HBS formulation was bioequivalent with Sinemet CR with respect to levodopa, but it exhibited a moderately higher fluctuation index compared to Sinemet CR as a result of somewhat higher Cmax and lower Cmin values for the Madopar HBS formulation. 3-OMD (a metabolite of levodopa) levels were significantly (p < 0.05) higher for Madopar HBS and Madopar compared to Sinemet CR. The higher 3-OMD levels for the levodopa/benserazide combinations are consistent with a more potent decarboxylase inhibitory activity of benserazide as compared to carbidopa. The number of adverse events was highest for conventional Madopar (n = 18) compared to the controlled-release formulations (n = 12 for Sinemet CR and only 2 for Madopar HBS). A more efficient inhibition of dopamine formation from levodopa (resulting in higher 3-OMD levels) by Madopar HBS was consistent with the superior tolerability (especially for initial nausea) observed for the Madopar HBS formulation as compared to Sinemet CR.
sinemet drug class
PD was induced by administration of reserpine (5 mg/kg/day, i.p for 5 consecutive days), haloperidol (1 mg/kg, i.p.), and tacrine (2.5 mg/kg, i.p.) in experimental animals. The symptoms of PD such as tremors, akinesia, rigidity, catalepsy, and vacuous chewing movements (VCMs) were evaluated. Foot shock-induced aggression (FSIA) model was used to confirm anti-parkinsonian activity. The methanolic extract of Beta vulgaris (MEBV) was administered at doses of 100, 200, and 300 mg/kg, p.o. The combination of L-dopa and carbidopa was used as a standard drug. Behavioral studies such as locomotor activity and grip strength were determined, and oxidative stress was evaluated in FSIA model in rat brain.
Continuous duodenal levodopa infusion (DLI) is an effective therapy that improves quality of life (QoL) in advanced Parkinson's disease (PD). However, the impact of DLI on caregivers' stress and burden has not been reported.
sinemet usual dosage
A primate model of Parkinson's disease was obtained by i. v. administration of 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP). A behavioural, a mechanographic and an electromyographic (EMG) study were carried out during the execution of a rapid elbow movement, in two normal monkeys and, after the MPTP administration, before and after a L-DOPA therapy. Disturbances in behavior, movement parameters and EMG activity observed in MPTP-treated monkeys mimic those reported in Parkinsonian patients. Treatment with L-DOPA was effective in greatly correcting these disturbances. These results lend weight to the assumption that use of MPTP in primate provides a good model to study Parkinson's disease.
Serum prolactin (PRL) level was assessed after challenges with apomorphine hydrochloride, saline, dopamine hydrochloride, or levodopa-carbidopa (Sinemet) in 19 control and 38 chronic schizophrenic subjects. Baseline PRL level varied inversely with age. High correlations existed between baseline PRL level and any subsequent absolute measure of PRL after administration of a dopamine agonist or placebo. Percent decrease was not a function of baseline concentrations and was therefore the only independent measure of drug response. Baseline PRL level was generally lower during exacerbation than remission in patients studied during two states of illness. Percent PRL level decrease after apomorphine administration was significantly greater in normal subjects than in schizophrenics. Correction of apomorphine responses for corresponding placebo (saline) values abolished differences between groups. Prolactin responses after dopamine or levodopa-carbidopa did not differ; however, placebo correction was not possible.
sinemet 50 mg
Burning mouth syndrome has been reported as being more common in Parkinson's disease patients than the general population. While the pathophysiology is unclear, decreased dopamine levels and dopamine dysregulation are hypothesized to play a role. We report a patient with Parkinson's disease who developed burning mouth syndrome with carbidopa/levodopa. Our patient had resolution of burning mouth symptoms when carbidopa/levodopa was replaced with a dopamine agonist. Based on our patient's clinical course, in conjunction with earlier studies assessing the relationship between burning mouth syndrome and Parkinson's disease, we discuss a potential role for dopamine in burning mouth syndrome in Parkinson's disease.
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Therapeutic responses to Sinemet CR were studied in 37 patients with early Parkinson's disease previously treated with standard (Madopar) or controlled-release (Madopar HBS) levodopa/benserazide combinations. Patients were followed up for a 3-month period. The optimal therapeutic response of parkinsonian disability to Sinemet CR was equal to that obtained with Madopar or Madopar HBS. The optimal therapeutic dosage of Sinemet CR was equal to that of Madopar HBS but 12% higher than that of standard Madopar. However, with Sinemet CR treatment, the number of daily doses needed was significantly fewer than with both previous treatments. End-of-dose failure, which had developed in 4 patients, and peak-dose dyskinesias present in 6 patients during treatment with standard Madopar, improved significantly with Sinemet CR. Thus, Sinemet CR seems to be beneficial and useful in the treatment of early Parkinson's disease.
sinemet drug components
Some investigators have proposed that Parkinson's disease (PD) patients often exhibit a worsening of tremor before the emergence of levodopa-induced dyskinesia (LDD). It is not clear, however, whether the presence of tremor depends on the severity of dyskinesia, nor is the precise time course of tremor relative to dyskinesia well understood. This report describes an objective study of the relationship between postural tremor and dyskinesia in eight PD patients who showed signs of choreoathetoid hand movements after a single dose of levodopa. Spectral analysis of sustained hand force provided an objective and sensitive method of detecting worsening of tremor in patients with LDD. Severity of clinical symptoms was highly correlated with severity of dyskinesia. Six of the patients exhibited increased tremor amplitude within 45 min of exposure to levodopa, with two of the six patients experiencing bilateral and four of the six having unilateral worsening of postural tremor. Tremor was more severe on the side with the more severe dyskinesia. These findings provide objective support for the notion that dyskinesia and postural tremor may stem from a common pathophysiologic mechanism.