Profile of levodopa-induced dyskinesia in patients of Parkinson’s disease: a record based study (original) (raw)
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Predictors of Levo-dopa induced Dyskinesias in Parkinson's Disease
Annals of Indian Academy of Neurology, 2019
IntRoductIon Parkinson's disease (PD) is one of the most common neurodegenerative diseases encountered in clinical practice. Increased awareness and access to quality health care have seen a greater number of patients on Levodopa treatment in India. The initial solace patients and treating doctors' experience due to the exquisite response to levodopa gives way to despair with the onset of disabling dyskinesias. Invariably, most PD patients go on to develop levodopa-induced dyskinesias (LID). [1] However, some patients develop early or severe disabling dyskinesias. The factors deciding which subset of PD patients go on to develop early or severe disabling dyskinesias are less clear. Dyskinesias can vary in type and severity. The management of LID also depends on the same. We undertook this study to analyze the clinical profile, disability, and predictors of LID. mateRIals and methods This was a cross-sectional observational study conducted in the Department of Neurology, Government Medical College, Thiruvananthapuram. Consecutive patients with PD (The UK PD Brain Bank Clinical Criteria), attending our movement disorder clinic, were included in the study after obtaining the Institutional Ethics Committee approval. Patients on levodopa treatment with a minimum follow-up of 6 months were included in the study. Patients on antipsychotics, those with alternative causes for dyskinesia, and who had premorbid dyskinesia were excluded from the study. The predictors of LID in patients with PD were studied and analyzed. We also examined the clinical profile and effect of LID on activities of daily living (ADL). After obtaining written informed consent, the patient's demographic details and clinical information including disease duration, duration of treatment with levodopa, the total dose of levodopa per day, and drugs currently used were noted. Video recordings of dyskinesias were analyzed for classification. [2] The modified Hoehn and Yahr stage, [3] Unified PD Rating Scale Part III, Unified Dyskinesia Rating Scale, [4] and PDY-26 item questionnaire were recorded. All patients were observed before and after administration of levodopa to assess onset, Background: Levodopa has a superior antiparkinsonian effect than dopamine agonists making it the standard of care for patients with Parkinson's disease (PD). During the initial stages, PD patients show a steady response to levodopa. Response fluctuations and levodopa-induced dyskinesias (LID) develop subsequently. The timing and onset of dyskinesias vary among individuals, and there are very few studies identifying the predictors of dyskinesia in India. Aims: We aimed to study the clinical profile, disability, and predictors of LID in a patient with PD. Materials and Methods: This was a cross-sectional observational study of consecutive patients with PD attending our movement disorder clinic. Patients on levodopa treatment with a minimum follow-up of 6 months were included in the study. All patients were observed before and after administration of levodopa to assess onset, duration of action, and timing of dyskinesias. Dyskinesias were video recorded and classified. Bivariate analysis was performed using Chi-square test or Fisher's exact test and multivariate analysis using binary logistic regression. Results: This study recruited 110 patients with PD on levodopa therapy. Thirty-one (28.1%) out of 110 had LID. Of these, 25 patients (80.6%) had on-time dyskinesia, 19 patients (61.3%) had off-time dystonia, and 13 patients (41.9%) had diphasic dyskinesia. Majority had only mild-to-moderate dyskinesia. Incapacitating dyskinesias were during off time, primarily affecting the foot. Age, disease duration, disease severity, duration of treatment, and total dose of levodopa were found to be predictors of LID. Multivariate regression analysis showed younger age and longer duration of levodopa treatment to be independent predictors for LID. Conclusions: LID is fairly common in PD though not severely disabling. Patients with younger age of onset, longer disease duration, and severe disease were more likely to get early LID. We observed the lower prevalence of LID when initiating at lower doses and slow titration of levodopa.
Levodopa-induced dyskinesia in Parkinson disease
Neurology, 2018
Objective To assess dyskinesia frequency in a population-based cohort of patients with Parkinson disease (PD). Dyskinesia complicates levodopa treatment and affects quality of life. Methods Utilizing the 1991-2010 population-based, parkinsonism-incident cohort of Olmsted County, MN (n = 669), accessed via the Rochester Epidemiology Project, we identified patients with PD and abstracted levodopa-related dyskinesia information. Results Of 309 patients with PD (46.2% with parkinsonisms), 279 (90.3%) received levodopa. Most (230/279; 82.4%) had been treated by a Mayo Clinic neurologist. Median age of the 309 patients with PD at the time of diagnosis was 74.1 years (range 33.1-97.8 years). Median-age levodopa initiation in this cohort was 75 years (range 37-98 years), and median-duration levodopa treatment was 6 years (range 2 months to 19.8 years). Dyskinesia was documented in 84 of 279 patients (30.1%). Median time from levodopa initiation to dyskinesia onset was 4 years (range 2 months to 20 years); those with dyskinesia (65.5%; 55/84) developed it within 5 years of levodopa initiation (9 within the first year). Dyskinesia was mild in 57/84 (67.9%), moderate in 16/84 (19.1%), and severe in 9/84 (10.7%); severity was not reported in 2 cases. Dyskinesia severity led to levodopa adjustments or amantadine initiation in 60.7% (51/84 of those with dyskinesia), with improvement in 23/51 (45.1%). Thirteen patients with dyskinesia underwent deep brain stimulation, reporting marked improvement. Postmortem examination confirmed Lewy body disease in 7 autopsied cases. Conclusions Levodopa-induced dyskinesia affected 30% of the patients with PD in our cohort. Mayo neurologists favoring levodopa dosage optimization treated most patients. Dyskinesia was severe in 3.2% of all levodopa-treated patients with PD (10.7% of all patients with dyskinesia) with marked improvement among those treated with deep brain stimulation.
Levetiracetam for the management of levodopa-induced dyskinesias in Parkinson's disease
Movement Disorders, 2010
The efficacy and safety of levetiracetam (LEV), administered for management of levodopainduced dyskinesias (LID) in Parkinson's disease (PD), was examined using a multicenter, double-blind, placebo-controlled, parallel groups, crossover trial. Because of having a period effect, data after crossover point was excluded from analysis. Levodopa-treated PD participants with LID (n 5 38) received LEV 500 mg/ day, were assessed, titrated to 1,000 mg/day and reassessed, before and after crossover. The placebo group followed the same routine. Primary efficacy was defined from percent change in ''On with LID'' time from patient diaries. Secondary efficacy assessment used ''On without LID,'' ''Off'' time, unified PD rating scale (UPDRS), clinical global impression (CGI), and Goetz dyskinesia scale after levodopa challenge. Safety measures were also performed. On with LID time decreased 37 minutes (95% confidence interval [CI] 0.59, 7.15; P 5 0.02) at 500 mg/day, 7.85% 75 minutes (95% CI 3.3, 12.4; P 5 0.002) at 1,000 mg/day. On without LID time increased by 46 minutes (95% CI 21.55, 20.03; P 5 0.04) at 500 mg/day and 55 minutes (95% CI 210.39, 21.14; P 5 0.018) at 1,000 mg/day. UPDRS 32 showed decreased dyskinesia duration mean change 0.35 (95% CI 0.09, 0.5; P 5 0.009) at 1,000 mg/day. CGI showed LID decreased by 0.7 (95% CI 0.21, 1.18; P 5 0.006) at 1,000 mg/day. Patient diaries and UPDRS show no increase in Off time. This exploratory trial provides evidence that LEV in 1,000 mg/day, slowly titrated, could be useful in improving LID as was assessed with patient diaries, UPDRS, and CGI scales, safely, with minimal side effects. V
Clinical Aspects and Management of Levodopa-Induced Dyskinesia
Parkinson's Disease, 2012
In Parkinson's disease, one of the most troublesome dilemmas is the treatment of levodopa-induced dyskinesia. After a few years, chronic treatment with levodopa is associated with the development of dyskinesias. Strategies to delay or to reduce dyskinesias are based on the change of levodopa dosing or the early use of dopamine agonists. Dopamine agonists with different pharmacological profile are available. Our paper was aimed to analyse the clinical impact and the management of dyskinesias with dopamine agonists.
Movement Disorders, 2004
We report four patients with Parkinson's disease who had an unusual pattern of severe chorea and dystonia in the evenings only. The temporal pattern of abnormal movements and simultaneous monitoring of plasma levodopa and clinical state were consistent with dyskinesias associated with subtherapeutic (low dopa dyskinesias) rather than peak concentrations of levodopa (high dopa dyskinesias). In two patients, addition of a direct-acting dopamine receptor agonist was helpful in ameliorating this complication of anitparkinson therapy. Key Words: Parkinson's disease-Evening-Dyskinesias-Low dopa dyskinesias.
Postgraduate Medical Journal, 2007
Levodopa is the most effective drug for treating Parkinson's disease. However, long-term use of levodopa is often complicated by significantly disabling fluctuations and dyskinesias negating its beneficial effects. Younger age of Parkinson's disease onset, disease severity, and high levodopa dose increase the risk of development of levodopa-induced dyskinesias (LID). The underlying mechanisms for LID are unclear though recent studies indicate the importance of pulsatile stimulation of striatal postsynaptic receptors in their pathogenesis. The non-human primates with MPTP-induced parkinsonism serve as a useful model to study dyskinesia. Once established, LID are difficult to treat and therefore efforts should be made to prevent them. The therapeutic and preventative strategies for LID include using a lower dosage of levodopa, employing dopamine agonists as initial therapy in Parkinson's disease, amantadine, atypical neuroleptics, and neurosurgery. LID can adversely affect...
Movement Disorders, 2005
We evaluated the tolerability and preliminary efficacy of levetiracetam (LEV; Keppra) in reducing levodopa-induced dyskinesias in Parkinson's disease (PD) in an open-label pilot study. Nine PD patients who were experiencing peak-dose dyskinesias for at least 25% of the awake day and were at least moderately disabling were treated with LEV in doses up to 3,000 mg for up to 60 days. The primary outcome measure was the percent of the awake day that patients spent on without dyskinesia or with nontroublesome dyskinesia (good on time). The mean dose of LEV at endpoint was 625 ± 277 mg/day. LEV significantly improved percent of the awake day on without dyskinesia or with nontroublesome dyskinesia at endpoint compared to baseline (43% ± 12% vs. 61% ± 17%; P = 0.02). Percent on time with troublesome dyskinesia decreased from 23% ± 10% at baseline to 11% ± 6% at endpoint, although not significantly. There was no significant increase in off time from baseline to endpoint. There was a 56% dropout rate, mostly due to somnolence. In PD patients who experienced peak-dose dyskinesia for at least 25% of the awake day, LEV significantly improved on time without dyskinesia or with nontroublesome dyskinesia. © 2005 Movement Disorder Society
Journal of Parkinson's disease, 2012
Levodopa-induced dyskinesias (LID) belong to the most common dose-limiting adverse effects of levodopa therapy. "Peak-dose" LID occur with the maximum effect of medication, 'diphasic dyskinesias' have a "beginning- and end-of-dose" pattern, and the, "off-period dyskinesia" occur during off-periods, most frequently in the early mornings and are typically dystonic in nature. The majority of patients will have developed dyskinesias after 10 years of treatment, and about 40-50% after 5 years. Occurrence of LID appears to be related to dose and duration of treatment with levodopa and severity and duration of disease. In addition, patients with younger age of onset have been reported to have an earlier onset and higher rate of LID. The important aetiological role of non-physiological pulsatile stimulation of dopaminergic receptors is increasingly recognized and more continuous dopaminergic stimulation with the longer acting dopamine agonists has been ...
Levodopa-induced dyskinesia in Parkinson’s disease: still no proof? A meta-analysis
Journal of Neural Transmission, 2018
Levodopa-induced dyskinesia is normally assessed based on the course of the appearance of their symptoms. Diphasic dyskinesia (DD) usually appears at the beginning and at the end, but not at the peak, of the levodopa effect in long-term treated Parkinson's disease patients. The most commonly affected subjects with this form of dyskinesia are those who have an early onset of the disease, approaching 20 % of globally treated parkinsonian patients. Typically, they are present in the lower limbs and exhibit rhythmic and sometime stereotypic movement patterns. In the past, DD were a serious management problem and often associated with severe dysautonomic manifestations. Current pharmacological trends to avoid high levodopa use have reduced the incidence of very troublesome DD. When severe, surgical approach may be considered, since pallidotomy typically resolves the movements. In a broader sense, the net predominance of the lower limb in DD is a fascinating mystery of which resolution could lead to important advances in the functional anatomy of the basal ganglia and Parkinson's disease.