View clinical trials related to Tardive Dyskinesia.
Filter by:Tardive dyskinesia (TD) is a well-known complication of antipsychotic drug therapy in individuals treated for mental disorders such as schizophrenia. It typically consists of purposeless, involuntary movements involving the mouth area or the trunk and limb muscles, occurring within months or years of drug use. The annual incidence of TD in the population treated with antipsychotic drugs is between 1-5%, but the risk is 5-fold greater in older individuals. Once triggered, TD is often irreversible and untreatable. Its cause is unknown, but an imbalance between chaotic mechanisms triggered by the drugs and natural protective factors fighting against these may provide an explanation. One way to activate this protective response is to supplement the diet with high doses of essential fatty acids of the omega-3 class, which constitute a critical component of nerve cell membranes. Using this strategy, one research team showed a 50% reduction in the severity of TD-like movements in mice treated with docosahexaenoic acid (DHA). We hypothesize that DHA supplements can do the same in patients living with schizophrenia displaying TD movements. Forty (40) subjects between 30-75 years of age will be recruited. The participants will be randomized and equally distributed in two groups to take either DHA capsules (3 grams a day) or matching placebo for 12 weeks, after providing informed consent, and TD will be measured with a magnetic tracker system and clinical scales. The finding of a beneficial effect with DHA against TD would improve the quality of life for thousands of patients under long-term antipsychotic drug treatment.
The objective of the study is to determine whether Panax Ginseng with multiple interactions with key components of brain signaling pathway, can augment the effects of antipsychotics in Schizophrenia. We are primarily interested to examine the actions of Ginseng combined with antipsychotics in improving the ways patients diagnosed with schizophrenia behave in social environment, store, process and retrieve information.
This is a placebo-controlled study designed to learn if levetiracetam is effective for tardive dyskinesia.
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.
Tardive dyskinesia (TD), a form of movement disorder, remains a problem for some patients who received antipsychotic medications. Increasing evidence suggests that TD may result from antipsychotic-induced dysfunction in striatal cholinergic neurons. To test whether cholinesterase inhibitors compensate for diminished cholinergic activity underlying TD, we conducted a 30-week randomized, double-blind, placebo-controlled crossover study of galantamine in 36 patients with TD.