View clinical trials related to Dyskinesias.
Filter by:This study is a multicenter, prospective cohort study of patients diagnosed with primary ciliary dyskinesia, the clinical information of recruited patients, including clinical manifestations, lung function, chest imaging, quality of life and other indicators, will be followed for 10 years.
1. Assessment of a high speed video camera with a green light source for the measurement of ciliary beat frequency (CBF) in the nasal airways of patients. 2. Assessments of the effect of drugs and other therapies on CBF using the study system. 3. Comparison of results with standard methods such as ciliary brush biopsies
This is a randomized sham-controlled double-blind study to test the hypothesis that transcranial static magnetic field stimulation (tSMS) of the motor cortex improves levodopa-induced dyskinesias in patients with Parkinson's disease. Half of the patients will receive real tSMS treatment, the other half will receive sham treatment (placebo).
This is a multi-centre, single visit clinical investigation involving patients with known PCD vs. age matched healthy volunteers. This study involves 1 visit which will last one (1) to two (2) hours. Participants (and parent as applicable) will be asked for their consent to participate in the study. A brief medical history will be recorded, including information such as age, gender, height, weight, race, current medications and living environment. If the participant is a PCD patient, they will also be asked about their disease history. Prior to performing the nasal measurements, participants will receive instructions from study personnel and have the opportunity to practice. All participants will have a brief nasal exam and will also have to blow their nose before starting the measurements. Participants will be asked to perform nasal nitric oxide measurements using the tidal breathing method followed by the velum closed with expiration against resistance method. The primary objective is to determine the feasibility and capability of the NIOX VERO to discriminate participants with PCD from those that are healthy. Information collected in this study will help researchers understand more about the diagnosis of and identification of patients with PCD.
Parkinson's disease (PD) is one of the most common neurodegenerative diseases, with a higher prevalence in the elderly. Levodopa induced dyskinesias (LID) are a major motor complications that impair quality of life for patients with PD. The mechanisms of these dyskinesias remain unclear, but several hypotheses have been put forward: non continuous, pulsatile stimulation of dopaminergic receptors, or alterations of other neurotransmitters within the motor striatum such as glutamate and serotonin. Few strategies are now available to treat severe LID: - Medications: reduction of dopaminergic treatment, addition of amantadine, - Functional neurosurgery. The purpose of this study is to investigate the efficacy of buspirone in PD patients suffering from dyskinesias. The role of serotonin in the occurrence of LID was recently demonstrated in transplant PD patients and a test double-blind, single dose was achieved. Following administration of 10 mg oral buspirone, a 5HT1A agonist, LID were clearly improved. A antidyskinetic effect of buspirone had already been reported in 1991 and 1994, but identification of buspirone as a serotonin receptor agonist has been reported more recently. This trial is aimed at (1) validate the serotoninergic hypothesis of hyperkinetic levodopa induced dyskinesias (LID) in Pakinson's disease patients, (2) evaluate, in a phase 3 trial, the motor efficacy of buspirone to improve LID vs placebo, (3) look at a possible dose/effect relationship and (4) check the hypothesis of a better therapeutic ratio using the association of buspirone and amantadine instead than a single drug.
The primary objective of this study is to evaluate the efficacy of buspirone in combination with amantadine in reducing levodopa-induced dyskinesia (LID) in patients with Parkinson's disease (PD).
Background: Patterns of scapular dyskinesis have unique scapular kinematics and associated muscular activation. The characteristics of scapular dyskinesis may be associated with functional disability. The investigators investigated whether the level of shoulder function and primary dysfunction items were different in each unique pattern of scapular dyskinesis. The factors associated with shoulder dysfunction in different patterns of scapular dyskinesis were identified. Methods: Participants with unilateral shoulder pain were classified as having a single dyskinesis pattern (inferior angle prominence, pattern I; medial border prominence, pattern II) or a mixed dyskinesis pattern (patterns I+II). Clinical measurements with the Flexilevel Scale of Shoulder Function (FLEX-SF score), shoulder range of motion, anterior/posterior shoulder tightness, and pectoralis minor index were recorded. These clinical measurements, 3-D scapular kinematics (electromagnetic-based motion analysis), and associated muscular activation (electromyography on the upper, middle, and lower parts of the trapezius and serratus anterior muscles) during arm elevation were analyzed for associations with functional disability.
The aims of this proposal include tests of hypotheses of the pathogenetic mechanisms of noradrenergic neurotransmission in Parkinson's disease in vivo, using positron emission tomography of patients with early and advanced Parkinson's disease with or without 3,4 L-dihydroxyphenylalanine (L-DOPA) - induced dyskinesia or co-morbid depression, and evaluation of whether these mechanisms can be influenced therapeutically. Hypotheses: 1. The investigators argue that release in human cortical and subcortical brain regions of norepinephrine (NE) derived from metabolism of exogenousL-DOPA is greater in Parkinson's disease patients with L-DOPA- induced dyskinesia than in patients without this complication. This hypothesis will be tested by measuring antagonist [11C]yohimbine binding to alpha-2 adrenoceptors before and after L-DOPA challenge. 2. If so, it is argued that the greater rise of norepinephrine, measured as [11C]yohimbine displacement after L-DOPA challenge, is the result of down-regulation or loss of norepinephrine transporters. This hypothesis will be tested by measuring the binding of [11C]MeNER, a tracer of norepinephrine transporters. 3. If so, the investigators argue that the greater decline of [11C]MeNER binding is significantly correlated to the symptoms of Parkinson's disease, as proof that patients with more severe loss of noradrenergic terminals exhibit more severe motor deficits.
Rationale: Tardive dyskinesia and dystonia (TDD) are severe side effects of dopamine blocking agents, particularly antipsychotics. Deep brain stimulation (DBS) has shown to be effective in the treatment of TDD in psychiatric patients, but only reported in case reports and small clinical trials and with little attention to possible psychiatric or cognitive complications or positive effect on psychiatric symptoms. Objective: To assess whether treatment with DBS can reduce or resolve TDD and if DBS can induce beneficial or side-effects in particular psychiatric symptoms. Study design: A delayed onset double blind randomised controlled trial. Study population: Adult patients with a current or previous psychiatric disorder and antipsychotic induced TDD with a stable psychiatric status during the past 6 months. Intervention: All patients will be treated with DBS in the posteroventrolateral GPi. The groups will be randomised into immediate stimulation or delayed stimulation after 3 months. Main study parameters/endpoints: Primary objective, improvement on the movement rating scales BFMDRS. Secondary objectives improvement on the quality of life measured on the SF-36, psychiatric stability as measured on the BPRS and the MADRS and cognitive effects as measured on the MATTIS Dementia Rating Scale, Nederlandse Leestest voor Volwassenen (NLV), 15 word test, Facial Expression of Emotion S+T (FEEST), Groninger Intelligentie Test woordopnoemen (GIT), category and letter fluency test, Trail Making Test part A and B and the Stroop colour and word test
The purpose of a randomized, double-blind, placebo-controlled, 2-way crossover study is to evaluate the efficacy, safety/tolerability and pharmacokinetics of JM-010 for the treatment of subjects with Parkinson's Disease (PD) with levodopa-induced dyskinesia (LID).