Drug-induced thrombocytopenia can be caused by various medications and should be suspected in any patients with newly developed thrombocytopenia. We report a patient with severe thrombocytopenia induced by L-dopa. This is the first case report on L-dopa-induced thrombocytopenia in Korea.
Humans ; Levodopa ; Thrombocytopenia

Patients with Parkinson disease （PD） can have hand and foot deformities called “striatal deformities”， which often occur in the middle and late stages of PD， but also in the early stage. The clinical manifestations of such deformity are similar to those of hand-foot deformity due to osteoarticular diseases， and some patients may have pain and discomfort； however， the low incidence rate and few reports of this disease may easily lead to misdiagnosis and mistreatment.
Parkinson Disease ; Levodopa

Objective To investigate the clinical features of dyskinesia and related risk factors in female patients with Parkinson disease （PD）. Methods A cross-sectional study was conducted among the female patients who met the diagnostic criteria for PD at the outpatient service of PD in Aerospace Center Hospital， and demographic data and clinical data were collected and compared between groups， including levodopa equivalent daily dose （LEDD）， Unified Parkinson’s Disease Rating Scale-Ⅲ（UPDRS-Ⅲ）， UPDRS-Ⅳ， scores of non-motor symptoms （cognition and depression）， presence or absence of dyskinesia， and single levodopa dose （LD） during the onset of dyskinesia. A binary logistic regression analysis was used to investigate the influencing factors for dyskinesia in female patients with PD. Results A total of 146 female PD patients were enrolled， among whom 30 patients had dyskinesia， with an incidence rate of 20.5%. Compared with the non-dyskinesia group in terms of clinical features， the dyskinesia group had a significantly younger age of onset [（54.3±12.5） years vs （62.7±10.0） years， P<0.001]， a significantly longer disease duration [（9.9±3.7） years vs （4.5±3.7） years， P<0.001]， a significantly higher severity of disease [H-Y stage： （2.65±0.58） vs （2.35±0.83）， P=0.03]， a significantly longer duration of LD administration [（7.5±3.2） years vs （3.2±2.6） years， P<0.001]， a significantly higher LEDD [（703.2±203.9） mg vs （442.1±226.3） mg， P<0.001]， and significantly lower body weight [（54.1±8.2） kg vs （60.0±8.7） kg， P=0.001] and BMI [（20.9±3.1） kg/m2 vs （23.4±3.1） kg/m2， P<0.001]. The multivariate logistic regression analysis showed that high BMI （OR=0.770， P=0.005） was a protective factor against dyskinesia in female PD patients， while long disease duration （OR=1.304， P=0.001） and high LEDD （OR=1.003， P=0.012） were risk factors for dyskinesia. Conclusion There is a relatively high incidence rate of dyskinesia in female PD patients， which should be taken seriously in clinical practice， and high BMI is a protective factor， while long disease duration and high LEDD are risk factors for dyskinesia in female PD patients.
Parkinson Disease ; Dyskinesias ; Levodopa

Parkinsonism associated with obstructive hydrocephalus due to idiopathic aqueductal stenosis or after shunt revision has been occasionally reported in the literature. Their Levodopa effectiveness and good prognosis has also been reported. However, the etiology and pathophysiology has not been well elucidated. We herein report two cases of parkinsonism associated obstructive hydrocephalus due to SAH. Interestingly, in both cases, parkinsonism occurred after a V-P Shunt and not after obstructive hydrocephalus.
Hydrocephalus* ; Levodopa ; Parkinsonian Disorders* ; Prognosis

Depression is frequently accompanied in idiopathic Parkinson's disease, and there were many researches about the pathogenetic mechanism of the depression. Recently the depression is thought to be developed by endogenous mechanism or reactive mechanism. To investigate the relationship between the changes of depression and the responsiveness of movement symptoms to the levodopa therapy, the UPDRS and BDI were checked before and after treatment of long-tem levodopa treatment. After levodopa treatment, the UPDRS was significantly improved but the depression was not improved. The depression severity in patients with Parkinson's disease were not influenced by the age, sex, symptom duration, treatment duration and the improvement of movement symptoms. And there were no differences in the clinical features between the levodopa responsive group and levodopa unresponsive group. Any clinical parameters do not predict the responsiveness of the depression to the levodopa therapy. These results suggest that the depression in Parkinson's disease, if it is endogenous, is related to neurochemical systems other than dopaminergic, or if it is reactive, is seldom influenced by drug-induced symptomatic improvement.
Depression* ; Humans ; Levodopa* ; Parkinson Disease*

No abstract available.
Levodopa* ; Neuroleptic Malignant Syndrome* ; Parkinson Disease*

We evaluated the therapeutic effects and complications of 118 patients with idiopathic parkisonism who were receiving levodopa therapy for more than 1 year. Response to therapy and complications of drug were correlated with duration of the disease and with duration of the treatment. Patients with motor fluctuation were likely to have been treated for 3 years or longer. Patients treated with levodopa for 5 years or longer were significantly more impaired with parkinsonism than patients treated for 1 to 3 years. Our findings suggest that the deterioration of responsiveness after several years of levododpa therapy may be due to the therapy itself, and utilization of levodopa therapy should be delayed until a patient becomes significantly impaired in occupational or social situations.
Humans ; Levodopa* ; Parkinson Disease* ; Parkinsonian Disorders

30 patients with Parkinson’s, ages of more than 45 years treated by levodopa but clinical symptoms were unstable. Trivastal slowed the demand of increase of dose of levodopa when combining with levodopa. The adequate dose of trivastal was 1 tablet/day within 15 days, then increased to 2 tablets/day. The drug usually had an effect in 45th day, mainly on the improvement of tremble and speaking difficulty.
Parkinson Disease ; Piribedil ; Levodopa ; therapeutics ; Pharmaceutical Preparations

To evaluate P300 cognitive evoked-potential, the pattern of learning impairment and their possible relationship in patients with idiopathic Parkinson's disease, we performed P300 cognitive potential test and neuropsychologic tests evaluating learning ability-Gollin's incomplete drawing test (GIDT) , the tower of Hanoi Puzzle (TOHP), and recall the name of pictures in Gollin's incomplete drawing test (GIDT recall), on 37 patients with idiopathic Parkinson's disease (19 never-medicated and 18 with levodopa therapy for more than 6 months) and age- and sex-matched normal healthy controls. Compared with controls, patients showed significant delay in P300 latency and significant impairment in TOHP and GIDT recall, but not in GIDT. The revodopa-treated patients showed significantly shorter P300 latency and better performance in TOHP than never-medicated patients, although they still showed impairments in both tests compared with controls. Although all neuropsychologic tests used in present study significantly correlated to the P300 latency in patients, the most significant correlation was found in TOHP. These results suggest, first, the P300 latency significantly delayed in parkinsonian patients which is partially improved by levodopa therapy ; second, visuomotor procedural learning but not visuoperceptual procedural learning is impaired in parkinsonian patients which is also partially responsive to levodopa therapy third, although visuoperceptual procedural learning is not impaired, the transformation process of procedural learning into declarative learning is probably impaired in Parkinson's disease ; fourth, the dopaminergic lesion in Parkinson's desease may have a role in producing both P300 abnormality and impairments in visuomotor procedural learning.
Humans ; Learning* ; Levodopa ; Neuropsychological Tests ; Parkinson Disease*

Bromocriptine(15-100 mg/day) alone and with L-dopa were studied for 10-30 months on 22 patients with Parkinson's disease. Patients who had never received L-dopa treatment either because it was never attempted or of intolerance from the onset was placed under Bromocriptine. The responses of patients were excellent. Its antiparkinsonism activity in comparable with that of L-dopa with the advantage of reducing the unwanted side effects of L-dopa during the reduction of its dosage, for patients who have been taking the drug. However, this decrease of dosage should be effected gradually, while the dose of Bromocriptine in being increased. Bromocriptine did not treat the "on-off" effects of L-dopa but reduced the cardiac complications, painful contractions and dyskinesia.
Bromocriptine* ; Dyskinesias ; Humans ; Levodopa ; Parkinson Disease*