View clinical trials related to Dyskinesias.
Filter by:Mucociliary clearance, in which mucus secretions are cleared from the breathing airways, is the primary defense mechanism for the lungs. Inhaled particles, including microbes that can cause infections, are normally entrapped in mucus on the airway surfaces and then cleared out by the coordinated action of tiny hair-like structures called cilia. Individuals with primary ciliary dyskinesia, variant cystic fibrosis, and pseudohypoaldosteronism have defective mucociliary clearance. The purpose of this study is to collect clinical and genetic information about these three airway diseases to improve current diagnostic procedures.
The primary purpose of the study is to investigate the anti-dyskinetic effect of several doses of sarizotan in Parkinson patients in order to generate information on the dose-response relationship (dose-finding).
TD is a troublesome and potentially irreversible side effect associated with the use of neuroleptics. While the newer neuroleptics are improved in this regard, they all still carry the risk of TD. The present study proposes that sarizotan is a potential agent for treating neuroleptic-induced TD based on preliminary data indicating efficacy in the management of dyskinesias associated with Parkinson's disease. Its efficacy is further substantiated by pre-clinical data obtained from the vacuous chewing movement (VCM) model in rats, a model we employ ourselves in investigating the relationship between D2 occupancy and TD. The present study also examines the effects of sarizotan on cognitive function, given the association between TD and cognitive deficits.
The study is designed to measure the efficacy and safety of levetiracetam on levodopa-induced dyskinesias in late-stage Parkinson's disease. The patients are planned to be treated with levetiracetam (up to 2000 mg per day) or placebo for 13 weeks. Efficacy measure is the modified AIMS.
A phase II double blind trial to evaluate the effects of the AMPA, glutamte antagonist, topiramate on levodopa-induced dyskinesia in Parkinson's disease
Levodopa-induced dyskinesias have been associated with irregular oscillatory discharge characteristics of basal ganglia. From the other hand, LEV which shares a different electrophysiologic profile than other antiepileptics, inhibits hyper-synchronization of abnormal neuronal firing in experimental models of epilepsy. LEV also reduces levodopa-induced dyskinesias in MPTP-lesioned macaques and modulates "priming phenomenon" which associated with long-term changes in synaptic function that can lead to dyskinesias in PD. Study objectives : - To evaluate the effects of levetiracetam (LEV) in two doses (500 and 1000mg) vs placebo on disabling dyskinesias that develop as result of long-term treatment with levodopa, occurring at the time of maximal clinical improvement in patients with Parkinson's disease (PD). - To evaluate the safety of LEV in patients with PD and antiparkinsonian medication.
This is a placebo-controlled study designed to learn if levetiracetam is effective for tardive dyskinesia.
This study will assess the risk of experiencing tardive dyskinesia and other movement disturbances associated with three atypical antipsychotic drugs among middle-aged and elderly psychiatric patients.
The mechanism involved in the development of tardive dyskinesia (TD) is complicated. It now seems that several neurotransmitter systems may be affected, including dopaminergic, noradrenergic, gamma-amino-butyric acid (GABA) ergic, cholinergic and peptidergic pathways. Piracetam (2-oxo-pyrrolidone) is a nootropic drug structurally related to GABA. It has been used clinically to treat a wide range of diseases and conditions, mainly in treatment of organic brain syndrome, myoclonus, memory impairment, post-concussional syndrome, vertigo, alcohol withdrawal, cerebrovascular insufficiency, hypoxia, intoxications of different origins or mechanic brain injures. Piracetam is cerebral homeostatic normalizer, neuroprotectant, cerebral metabolic enhancer and brain integrative agent. It enhances brain energy, especially under deficit condition: hypoxia, chemical toxicity or impaired cerebral microcirculation; preserve, protect and enhance synaptic membrane and receptor structure and plasticity. It has various effects on glutamate neurotransmission on micromolar levels piracetam potentiates potassium-induced release of glutamate from hippocampal nerves. It is an oxidant agent and may be useful for treatment TD. Piracetam is among the toxicologically safest drugs ever developed even in mega doses. Data derived from some clinical reports have suggested that piracetam can improve symptoms and is effective agent for treatment of different movement disorders including acute neuroleptic induced extrapyramidal symptoms and TD. The doses that used for TD treatment varied from 800 mg/day to 24000 mg/day. According to these findings the symptoms of TD disappeared in the period of 3-7 days. To date there was only one double-blind crossover study regarding use of piracetam for treatment TD that was conducted almost 20 years ago. The findings of this study were impressive, but to our knowledge nobody reproduced these results.
An 8-week study to examine safety and efficacy of levetiracetam in patients with neuroleptic-induced tardive dyskinesia