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It is widely accepted that enduring parkinsonian symptoms are only evident if there are few remaining dopaminergic neurons in the substantia nigra and dopamine levels in the basal ganglia are very low [26,41]. In the present study, partial dopamine depletions were produced by infusing 6-OHDA bilaterally into the ventrolateral striatum as previously described [11,12,44]. Consistent with previous studies, behavioral deficits were detectable in rats with partial lesions with a simple fixed-ratio bar-pressing task. The present study demonstrated that these behavioral deficits were long-lasting, and that the sensitivity of this bar-pressing task could be increased by manipulating the level of difficulty of the task-higher fixed ratios were more sensitive to partial dopamine depletions. Deficits in rats with partial dopamine depletions could also be detected using non-automated neurological tests of parkinsonian symptoms developed for rats with severe unilateral dopamine depletions, but these deficits were transient and not as robust as those detected with the bar-pressing task. Oral Sinemet (L-DOPA:carbidopa) did not attenuate behavioral deficits related to partial dopamine depletions in this simple fixed-ratio bar-pressing task, but the present results suggest that Parkinson's patients might be identifiable earlier in the disease process, at a time when they could benefit from treatment with neuroprotective/neurotrophic agents. In addition, the results of the present study demonstrate that robust behavioral deficits may emerge with age. Mild dopamine depletions that were not detectable behaviorally at the time of the insult became clearly evident 10 months after the lesion with this bar-pressing task, and this may represent a more clinically relevant rodent model of Parkinson's disease.
The clinical cases described are characterized by rigidity, mutism and hyperthermia, with cutaneous pallor and diaphoresis. This symptomatology marks the "malignant neuroleptic syndrome" and can be found, at times, in parkinsonians on "drug holiday". The cases described, which comprehend patients with both disorders, lead us to a single pathogenetic hypothesis: a central dopaminergic impairment. Hyperthermia, secondary to functional hypothalamic deficiency, is maintained by defective heat dispersion due to the lack of cutaneous vasodilation.
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We conducted a prospective study of thyroid function in 46 patients with Parkinson disease and 46 age- and sex-matched controls with other neurologic disease. There was no statistical difference in serum thyroxine (T4) and T3 resin uptake (T3U) between the two groups. Neither the duration nor the quantity of L-dopa or carbidopa/L-dopa (Sinemet) therapy influenced these assessments of thyroid function. However, 3 of 46 Parkinson patients were hypothyroid, whereas none of 46 controls was hypothyroid. There was one hyperthyroid individual in each group. Early evaluation of thyroid function in all patients with Parkinson disease is recommended because of the unexpected frequency of hypothyroidism and because hypothyroid symptoms may be masked.
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Infusion of carbidopa/levodopa or levodopa through a duodenal tube can facilitate increased mobility and functional ability in individuals with Parkinson's disease when conventional drug therapy is unsuccessful in achieving desired outcomes. Therapy requires appropriate patient selection, ongoing assessment of the patient's physical and emotional needs and collaboration between the patient, nurses and physicians. Determining the amount of medication required to achieve the desired outcomes takes time. Implantable pumps may be a future strategy. Future research should focus on patient and family coping throughout hospitalization and at home so the emotional needs of this specific population can be met.
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In five patients with parkinsonism, the optimal dosage of a controlled-release levodopa/carbidopa preparation (CR-3) was three times higher than the dosage of Sinemet and produced higher plasma levodopa concentrations, but did not reduce the fluctuations in plasma levodopa or clinical response. Plasma levodopa concentrations were higher and clinical responses better before the first dose of the day with CR-3. CR-3 treatment benefited two patients, reducing the severity of off periods and off dystonia. Two patients were worse on CR-3 despite higher plasma levodopa levels than those adequate for clinical response to Sinemet or levodopa infusions. CR-3 could benefit a few severely affected patients, but it is necessary to understand the factors that affect absorption of levodopa from sustained-release preparations, as well as the consequences of prolonged elevation of plasma levodopa levels.
The objective of this study was to assess the efficacy, safety, and pharmacokinetics of XP21279-carbidopa in patients with Parkinson's disease who experience motor fluctuations compared with immediate-release carbidopa-levodopa tablets. XP21279 is a levodopa prodrug that is actively absorbed by high-capacity nutrient transporters expressed throughout the gastrointestinal tract and then rapidly converted to levodopa by carboxylesterases. XP21279-carbidopa sustained-release bilayer tablets were developed to overcome pharmacokinetic limitations of levodopa by providing more continuous exposure. Patients with motor fluctuations who required carbidopa-levodopa four or five times daily were optimized for 2 weeks each on carbidopa-levodopa four or five times daily and XP21279-carbidopa three times daily in a randomized sequence. Next, they received each optimized treatment for 2 weeks in a double-blind/double-dummy, randomized sequence. The primary outcome measure was change from baseline in daily off time at the end of each double-blind treatment period. All patients at 2 sites underwent pharmacokinetic analyses. Twenty-eight of 35 enrolled patients completed both double-blind treatments. The mean total daily off time was reduced from baseline by a mean (± standard error) of 2.7 hours (± 0.48 hours) for immediate-release carbidopa-levodopa and 3.0 hours (± 0.57 hours) for XP21279-carbidopa (P = 0.49). Among 11 patients who completed pharmacokinetic sampling on each optimized treatment, the percentage deviation from the mean levodopa concentration was lower (P < 0.05) for XP21279-carbidopa than carbidopa-levodopa. Both treatments had a similar incidence of new or worsening dyskinesias. XP21279-carbidopa administered three times daily produced a reduction in off time similar to that of carbidopa-levodopa administered four or five times daily, and the difference was not statistically significant. XP21279-carbidopa significantly reduced variability in levodopa concentrations compared with carbidopa-levodopa.
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With advancing age, there are changes in both cognitive functions and neurotransmitter metabolism. Dopamine plays a role in learning, memory, and related cognitive processes. We evaluated the effects of supplemental dopamine in precursor form (levodopa) on various aspects of memory in elderly normal volunteers in a controlled, double-blind study. Access to semantic memory and automatic processes were unaffected, but levodopa reliably facilitated effortful memory processing. Levodopa may be useful clinically in attenuating impairments in effortful cognitive tasks. Different neural systems probably mediate different forms of cognition.
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1. We compare the sensitivity and specificity of chosen outcome criteria in a placebo-controlled, randomised cross-over study of the efficacy of maintenance therapy with the levodopa/carbidopa combination (Sinemet Plus) alone. Patients were characterised by having idiopathic Parkinsonism with no overt fluctuations in control in relation to individual doses of medication. 2. The effect of omission of a morning dose of maintenance therapy on simple timed tests of mobility and manual dexterity, and on distance/time parameters of gait was studied in fourteen patients (aged 64 to 88 years). Measurements made 2, 4 and 6 h after morning active and placebo treatments were standardised by taking the pre-treatment measurement on that day as baseline. 3. In a linear model, which allowed for the structure of the study, neither the total time taken by each patient to get up from a chair, walk an individually set distance, turn, return to and sit in the chair, nor the rate of progress at fastening the same set of buttons, was sensitive to the treatment effect. 4. Three of the gait parameters, free walking speed, mean stride length and mean double support time, were sensitive to the treatment effect. Correction for the speed of each walk, caused some reduction in the sensitivity of stride length to treatment effect, but that of double support time remained. Speed, and double support time or stride length, appeared to be complementary in defining the treatment effect. 5. The linear modelling revealed the complexity of the treatment effect. Although active treatment, by comparison with placebo, increased free walking speed (P = 0.019), the more levodopa found in the plasma following treatment, (P = 0.0005) and the greater the increment in the concentration of its peripheral metabolite, 3-O-methyldopa (P = 0.006), the less the beneficial effect. This model may reflect reduced uptake into the brain and/or an adverse effect of parent drug or a metabolite. 6. The specificity of free walking speed for the treatment effect was good, as was that of mean stride length, after it had been corrected for speed of each walk, and of mean double support time, after correction for speed and incorporation of the change in lying blood pressure accompanying treatment into the model. 7. The measurements of gait parameters were ranked according to reliability.(ABSTRACT TRUNCATED AT 400 WORDS)
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Participants were enrolled from two phase III IPX066 studies and one open-label phase II study. Early PD patients were titrated to an appropriate dosing regimen while advanced patients started with regimens established in the antecedent studies. Adjustment was allowed throughout the extension. Clinical utility measures included the Unified Parkinson's Disease Rating Scale (UPDRS) and Patient Global Impression (PGI) ratings.
The LC-5 microtablets were bioequivalent to the LC-100 tablets in area under the curve (AUC) and maximum concentration in plasma (Cmax) for levodopa, and to the LB-100 tablets in AUC. The dispersible levodopa/benserazide formulation showed earlier time to Cmax and significantly higher Cmax for levodopa in plasma compared to the microtablets. Carbidopa showed larger interindividual variation in AUC and Cmax than levodopa, and the bioequivalence comparison LC-5/LC-100 for this compound did not reach the target. Nevertheless, comparison of 3-O-MD levels for LC-5/LC-100, assuming proportionality to levodopa levels, demonstrated bioequivalence.
Controlled-release carbidopa/levodopa 50/200 (SINEMET CR) and standard carbidopa/levodopa (SINEMET 25/100) were compared in a double-blind, six-month, crossover study involving 21 patients with chronic Parkinson's disease and motor response fluctuations. Daily dosage frequency was significantly reduced with SINEMET CR compared with SINEMET 25/100, while the daily amount of levodopa required with SINEMET CR was significantly greater. No significant differences in disability ratings, motor response fluctuations, or safety were detected during double-blind conditions. In the open-label, dose-finding phase of the study, SINEMET CR was superior to standard SINEMET 25/100 in patient ratings of percent "on" time (good motor function), clinical assessments of motor function, and activities of daily living. This finding resulted from a depreciation of the value of the "old drug" rather than an overestimation of the value of the experimental drug. This double-blind study also suggested that elderly male patients with Parkinson's disease derived the greatest benefit from SINEMET CR.
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In Study 1, 67 cocaine-dependent subjects were randomized in a 5-week, double-blind, placebo-controlled safety trial. Subjects received either placebo, or 400 mg L-dopa plus 100 mg of the peripheral decarboxylase inhibitor, carbidopa, in a sustained-release preparation (Sinemet CR). In Study 2, 122 cocaine-dependent subjects were enrolled in a 9-week, randomized, double-blind, placebo-controlled trial to compare placebo to 400/100 mg and 800/200 mg L-dopa/carbidopa treatments. Placebo or L-dopa were administered twice daily in both studies.
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A reliable multi-dimensional column chromatographic method employing amperometric detection using a carbon fibre microelectrode procedure was used for monitoring the plasma profiles and to evaluate the pharmacokinetics and bioavailability of levodopa (L-dopa) and carbidopa (C-dopa), after ingestion of oral formulations containing these drugs. The peak currents obtained for the different analytes were directly proportional to the analyte over the concentration range 0.02-4 micrograms ml-1. Using this method, the minimum detectable concentration was estimated to be 5 and 8 ng ml-1 for L-dopa and C-dopa, respectively. Recovery studies ranged from 93.83 to 89.76%, with a relative standard deviation of less than 7%. The study was carried out in two separate weeks on five healthy non-patient fasted male/female volunteers in the age range 20-37 years and weighing between 60 kg and 78 kg. The pharmacokinetic profile of two controlled-release products containing both L-dopa and C-dopa (Sinemet CR3 and CR4) was compared on the one hand and Sinemet conventional tablets on the other. The pharmacokinetic parameters, peak concentration (Cmax), the time taken to obtain this level (Tmax), elimination half-time T1/2, elimination rate constant (Kel), plasma level ratio, fluctuation index (FI) and the area under the time-concentration curve (AUC0-8), were investigated for each individual formulation. A comparison of the uptake of L-dopa from the conventional formulation showed that L-dopa entered the plasma and achieved peak levels higher than that of the controlled release formulations. However, it showed a much higher fluctuation index and the plasma concentrations were more stable with the controlled release formulations. The data also indicated a very low accumulation of both levodopa and carbidopa following repeated administration of the drugs, which was consistent with their relatively short half-lives (less than 2 h). In contrast, the half-life for the metabolite 3-orthomethyl dopa (3-OMD) is in the order of 13 h. As a result, there was an extensive accumulation of 3-OMD and its levels were significantly higher than those of levodopa or carbidopa upon repeated administration. Urine recoveries of the three analytes over one 8 h dosing interval showed that the majority of the excreted levodopa and carbidopa was recovered during the first 4 h, and there is proportionally greater excretion of the carbidopa dose than the levodopa dose.
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A 17-year-old male developed acute parkinsonism after obstruction of a ventriculoperitoneal shunt with subsequent hydrocephalus. Following a previous shunt replacement, he developed florid parkinsonism which was associated with Parinaud syndrome. The initial single-photon emission computed tomography of the brain using 99mTc-hexamethylpropylenamine oxime demonstrated decreased cerebral blood flow in the regions of the left caudate and putamen. The patient underwent shunt revision with minimal improvement and therefore levodopa/carbidopa (Sinemet 100/25) was administered. Subsequently, he experienced almost complete recovery which may have been correlated with probable improvement of the basal ganglia regional cerebral blood flow. Parkinsonism associated with ventriculoperitoneal shunt obstruction is a rare but reversible disorder that is responsive to shunt replacement and antiparkinsonian drug administration. Cerebral perfusion studies may prove to be of value in delineating the pathophysiology of this complication.
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Levodopa/Carbidopa, respectively, Levodopa/Benserazide is the most effective treatment for Parkinson's disease and during the progress of the disease, patients will inevitably need to be treated with it. Nonetheless, after a certain time period most of the patients experience side effects. Mainly disturbing are motor and non-motor fluctuations and dyskinesia. Numerous options from changing the medication regimen, to continuos dopaminergic drug delivery via apomorphine or Duodopa pumps and stereotactical interventions are available. The physician's responsibility is to choose the right therapeutic procedure for each timepoint of the patient's disease. In this review, we provide an up to date overview of the available strategies.
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Using high-performance liquid chromatography with electrochemical detection, we determined serotonin in plasma from parkinsonian patients being treated with L-3,4-dihydroxyphenylalanine or N-(DL-seryl)-N'(2,3,4-trihydroxybenzyl)hydrochloride plus L-3,4-dihydroxyphenylalanine ("Sinemet") and in serum from a blood bank, from "normal" persons, and a pooled specimen from a hospital clinical laboratory. The values obtained for the two groups of Parkinson's disease patients showed no significant difference. Long-term storage on solid CO2 was xhown to be an adequate technique for preserving samples. The mean (+/-SEAM) normal value obtained for serotonin in serum was 146 +/- 46 microgram/liter (n = 23), a result in harmony with that previously obtained [Clin. Chem. 20, 812 (1974)] by fluorometry. In comparison to other methods for measurement of serotonin in serum or plasma, we believe that the present scheme offers greater selectivity, sensitivity, and precision.
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It is generally assumed that parkinsonian patients perceive their need for antiparkinsonian drugs on the basis of emergent motor symptoms. We describe five patients in whom an apparent psychologic effect from levodopa prompted dosage escalation to the point of toxicity. Abstinence from dopaminergic drugs resulted in the appearance of drug-seeking behavior. Psychologic dependence on levodopa has not previously been reported, but appears to occur in a small subset of parkinsonian patients.
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Among PD patients with substantial "off" time, a majority were safely converted to IPX066. The sustained LD profile from the IPX066 formulation allowed an increase in LD dose accompanied by improved motor functions, without increased troublesome dyskinesia.
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Although not significantly different from oral levodopa treatment (P > .05) in the double-blind study, levodopa-carbidopa intestinal gel treatment resulted in a reduction from baseline in "on" time with troublesome dyskinesia (mean [standard deviation] hours: baseline = 3.1 [1.7], change from baseline to final = -1.8 [1.8], P = .014), increase in "on" time without troublesome dyskinesia (baseline = 7.4 [2.2], change = 4.4 [3.6], P = .004), and decrease in "off" time (baseline = 5.5 [1.3], change = -2.7 [2.8], P = .015). Similar trends were found in the open-label study. An increase in levodopa-carbidopa intestinal gel dose was not significantly correlated with increased "on" time with troublesome dyskinesia in either study (double blind: r = -.073, P = .842; open label: r = -0.001, P = .992). Adverse events were usually mild to moderate in severity and related to the gastrointestinal procedure.
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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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Seven patients with a sensorimotor peripheral neuropathy followed years later by extrapyramidal manifestations are presented. This appears to be a separate genetic disorder(s) from that described as Machado-Joseph disease. In five subjects, other relatives had similar multisystem involvement. None was of known Portuguese ancestry. The extrapyramidal syndrome was mainly parkinsonian. Pain was prominent in five subjects. In all cases, low or moderate doses of levodopa/carbidopa ameliorated both the pain and the parkinsonian features. In one patient, a randomized placebo-controlled trial of levodopa/carbidopa was found to significantly improve most symptoms and neurologic dysfunction scores related to the extrapyramidal syndrome.
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1. We have used gait analysis to investigate the efficacy of maintenance therapy with a levodopa/carbidopa combination in patients with idiopathic Parkinsonism, who do not have overt fluctuations in control in relation to administration of medication. 2. Fourteen patients (aged 64 to 88 years) receiving maintenance therapy with levodopa and carbidopa (Sinemet Plus) entered a placebo-controlled, randomised cross-over study of the effect of omission of a morning dose of active treatment on distance/time parameters of gait. Measurements made 2, 4 and 6 h after the morning treatment were standardised by taking the pre-treatment measurement on that day as baseline. 3. The mean increase in stride length (7%) and decrease in double support time (20%) on active treatment were small but statistically significant (P less than 0.0001, in each case), there being no significant placebo effect on either gait parameter (P = 0.69 and 0.08 respectively). Neither active nor placebo treatments had any significant (P greater than 0.45 in each case) effect on the lying, standing or postural fall in mean arterial pressure, measurements being made in the same temporal relation to the treatments as was gait. 4. In a generalised linear model, after allowing for the effect (P less than 0.0001) of intrinsic variability in pre-treatment speed as well as for structure of the study, nature of treatment had an effect on stride length over the whole walk, significant at P = 0.002. 5. Pre-treatment postural fall in mean arterial pressure was nearly as significant (P = 0.003) as the nature of treatment in the context of such a model: the greater the fall, the greater the increment in stride length seen following active or placebo treatment. This was probably explained by an acquired tolerance to the fall as the day progressed. 6. The major determinant (P less than 0.0001) of the change in double support time over the whole walk, after allowing for the structure of the study, appeared to be the post treatment mean arterial standing blood pressure. The lower the pressure, the shorter the double support time, and hence, the greater the tendency to a hurried gait. 7. Nature of treatment, when added into the models described in summary points 5 and 6, had no significant effect (P greater than 0.25, in each case).(ABSTRACT TRUNCATED AT 400 WORDS)
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A single evening dose of LCE 200 was associated with significantly better bioavailability compared with CR-LC 200. In line with increased bioavailability of levodopa, LCE 200 induced more nausea.
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Four healthy monkeys were injected with diluted MPTP solution continuously through peripheral veins. The behavioral changes of the monkeys were monitored with the Parkinson disease scale for monkeys. 18FDG-PET-CT scans for the whole brain were obtained before and 3 months after the injection of MPTP. The pathological and glucose metabolic changes of the brains were examined.
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We identified 21 patients with DHS and parkinsonism, 12 male, 9, female. The median age of DHS onset was 69 years (interquartile range: 63.6-77.5 years). This included 10 patients with Parkinson's disease (PD), 10 with MSA, and 1 with drug-induced parkinsonism. The DHS component of their disorder segregated into three different subgroups: dystonia-alone (12 patients); myopathy-alone (4 patients; focal cervical myopathy in 3 and generalized myopathy in one); coexisting dystonia and myopathy (5 patients; 3 generalized, 2 focal cervical myopathy).
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Controlled-release carbidopa/levodopa 50/200 (Sinemet CR) and standard carbidopa/levodopa (Sinemet 25/100) were compared in a multicenter double-blind trial involving 202 patients with advanced Parkinson's disease and motor response fluctuations. Treatment with Sinemet CR significantly reduced daily "off" time. According to both physician and patient global ratings, patients showed significant improvements with Sinemet CR compared to treatment with standard Sinemet. Patients preferred Sinemet CR treatment by a ratio of approximately 2 to 1. Daily dosing frequency was 33% less with Sinemet CR, while daily intake of levodopa required was increased by 25%. The safety profiles of the 2 formulations were similar. We conclude that Sinemet CR is superior to standard Sinemet for many patients with advanced Parkinson's disease, although it does not solve the problem of fluctuating motor performance.
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Sinemet CR, a controlled-release form of carbidopa/levodopa, was administered for 36 or 39 months to 8 patients with Parkinson's disease in an open-label study. On standard Sinemet each patient had experienced "wearing off" phenomena, and 5 had also experienced random "off" episodes. Daily "on" time, dyskinesia time, disability score, levodopa dosage requirement, and dosing frequency on Sinemet CR were compared with baseline values on standard Sinemet therapy. After both 3 and 36 or 39 months of Sinemet CR therapy, 5 patients showed increased daily "on" time compared with baseline. All 8 required fewer daily doses after 3 months on Sinemet CR, but only 3 were still taking fewer doses after 36 or 39 months. Disability scores remained essentially unchanged. Patients continued to elect to remain on Sinemet CR over the 3-year period, citing improved predictability of response and less severe and precipitous "off" episodes as the main reasons. This experience suggests that patient acceptance of Sinemet CR remains high. A modest improvement in "on" time can be achieved and maintained in some patients for as long as 3 years. However, as with standard Sinemet, dosing frequency for Sinemet CR may need to be gradually increased with time in order to maintain benefits achieved.
Response fluctuations in motor function, complicating long-term dopaminomimetic therapy of Parkinson's disease, may extend to the cognitive realm. To evaluate the effect of levodopa treatment both on attention as well as acquisition and retrieval of memory tasks, parkinsonian patients were examined neuropsychologically both while medicated with levodopa/carbidopa ("on") and when the medication's antiparkinsonian effect had worn off ("off"). Significant cognitive differences emerged only on the delayed recall of complex verbal materials, where patients when "on" performed better compared with their "off" state. Comparison of change scores across states (administration or withholding of levodopa/carbidopa between acquisition and retrieval, "off" to "on" or "on" to "off"), revealed no substantial differences as a function of dopaminomimetic therapy. These results support the view that slight changes in cognition are associated with dopaminomimetic therapy of Parkinson's disease, but that these changes may be task-specific.
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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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Neuroleptic malignant syndrome (NMS) continues to be an unpredictable and rare, but potentially fatal complication of antipsychotic medications. Presumptively linked to dopamine blockade, it nonetheless occurs in patients receiving newer atypical antipsychotics. The features of NMS, its pathophysiology, differential diagnosis, clinical course, risk factors, and morbidity and mortality are reviewed. Nonpharmacologic management centers on aggressive supportive care including vigilant nursing, physical therapy, cooling, rehydration, anticoagulation. Pharmacologic interventions include immediate discontinuation of antipsychotics, judicious use of anticholinergics, and adjunctive benzodiazepines. The utility of specific agents in actively treating NMS is reviewed. Bromocriptine and other dopaminergic drugs and dantrolene sodium have alternatively been considered without merit or efficacious. Guidelines for using these agents are presented. Electroconvulsive therapy, also somewhat controversial, is identified as a second line of treatment. Finally, management of the post-NMS patient is also reviewed.
The efficacy of low-dose bromocriptine mesylate administration (20 mg daily or less) was evaluated in a double-blind study. Nine of 16 individuals receiving bromocriptine completed the 40-week study. Modest, but significant, improvement was derived from bromocriptine therapy. Improvement was most evident in tremor. Maximum improvement was achieved with doses between 7.5 and 15.0 mg daily, with some decline in efficacy as doses approached 20 mg. Adverse effects were common, but were generally mild in severity. Our results suggest that bromocriptine in low doses may be an effective adjunct to carbidopa and levodopa (Sinemet) in the treatment of Parkinson's disease.
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The results suggest that increasing central catecholamine availability inhibits the normal prolactin response to exercise in the heat but does not alter performance, thermoregulation, or sympathetic outflow.
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This was a prospective case series.
We conducted a retrospective review of patient electronic health records at a Midwestern public medical center. After applying inclusion and exclusion criteria and evaluating the eligible records, we had a final sample of 89 separate surgical events for 67 discrete patients who had been diagnosed with Parkinson's disease, had undergone any type of surgery excepting Parkinson's disease surgeries, and were taking carbidopa-levodopa.
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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.
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The thiol homeostasis determines the redox milieu and thus scavenging of free radicals by antioxidants like glutathione (GSH). GSH is formed out of cysteine in combination with l-glycine and glutamine acid. An up regulation of free radical occurrence is looked upon as one key feature of chronic neurodegeneration. Levodopa (LD) is under suspicion to support synthesis of free radicals via the degradation of its derivative dopamine in abundant mitochondria. Objectives were to investigate the impact of LD on free cysteine turnover in plasma. 200mg LD/50mg carbidopa (CD) were administered to 13 patients with Parkinson's disease under standardised conditions. Plasma levels of LD and free cysteine were measured before, 60- and 80-min after the LD/CD application. Cysteine concentrations decayed, expectedly LD levels increased. Cysteine decrease may result from an up regulation of GSH synthesis to encounter augmented appearance of free radicals associated with LD turnover via mitochondrial monoaminooxidase.
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Tetrahydropapaveroline (THP) concentrations were measured in the urine of Parkinsonian patients receiving L-dopa-carbidopa (Sinemet) therapy, using a method that employs a separation scheme that selectively isolates THP from urine and utilizes the Pictet-Spengler condensation of THP with formaldehyde combined with high-performance liquid chromatography for identification and determination. The mean (+/- S.D.) recoveries of THP from normal urine with 0.2 pmol/ml added and from Parkinsonian patients' urines with 0.5 pmol/ml added were 48.6 +/- 5.7 and 44.6 +/- 3.1%, respectively. Three Parkinsonian patients who were receiving either 250, 750 or 1000 mg of L-dopa (as Sinemet) daily had 24-h urinary THP excretion levels of 989, 1017 and 1600 pmol, respectively.
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Dopa-responsive dystonia is a hereditary disease characterized by inadequate dopamine production. Autosomal-dominant cases result from mutations in the GCH1 gene, encoding guanosine triphosphate (GTP)-cyclohydrolase 1. The most common presenting manifestation is dystonia of a lower extremity, often worsening late in the day. The onset and clinical severity are variable, sometimes even within a single family. Gender effects on allele penetrance have been reported. We present a male toddler with dopa-responsive dystonia caused by an autosomal-dominant GCH1 mutation. Three other family members were also found to carry the mutation, with widely different functional consequences.