What is Tardive Dyskinesia ?
Tardive dyskinesia is a variety of dyskinesia (involuntary, repetitive movements) manifesting as a side effect of long-term or high-dose use of dopamine antagonists, usually antipsychotics. Other dopamine antagonists that can cause tardive dyskinesia are drugs for gastrointestinal disorders (e.g. metoclopramide) and neurological disorders. While newer atypical antipsychotics such as olanzapine and risperidone appear to have less dystonic effects, only clozapine has been shown to have a lower risk of tardive dyskinesia than older antipsychotics.
The term tardive dyskinesia was introduced in 1964. Dyskinesia refers to an involuntary movement. The effect of these drugs can be tardive, meaning the dyskinesia sometimes continues or appears even after the drugs are no longer taken

Cause of Tardive Dyskinesia
Despite the fact that tardive dyskinesia has existed for over 50 years, its etiology is poorly understood due to the limited research conducted on psychiatric drug side effects. The cause of tardive dyskinesia appears to be related to damage to the system that uses and processes the neurotransmitter dopamine. The most compelling line of evidence suggests that tardive dyskinesia may result primarily from neuroleptic-induced dopamine supersensitivity in the nigrostriatal pathway, with the D2 dopamine receptor being most affected. Neuroleptics act primarily on this dopamine system, and older neuroleptics, which have greater affinity for the D2 binding site, are associated with high risk for tardive dyskinesia.[2] The D2 hypersensitivity hypothesis is also supported by evidence of a dose-response relationship, withdrawal effects, studies on D2 agonists and antagonists, animal studies, and genetic polymorphism research.
Given similar doses of the same neuroleptic, differences among individuals still exist in the likelihood of developing tardive dyskinesia. Such individual differences may be due to genetic polymorphisms, which code for D2 receptor binding site affinity, or prior exposure to environmental toxins. Decreased functional reserve or cognitive dysfunction, associated with aging, mental retardation, alcohol and drug abuse, or traumatic head injuries, has also been shown to increase risk of developing the disorder among those treated with neuroleptics.
The available research seems to suggest that the concurrent prophylactic use of a neuroleptic and an antiparkinsonian drug is useless to avoid early extrapyramidal side-effects and may render the patient more sensitive to tardive dyskinesia. Since 1973 the use of these drugs have been found to be associated with the development of tardive dyskinesia (Crane, 1973). Since some of the symptoms of tardive dyskinesia can be interpreted as schizophrenia by doctors, they may prescribe additional neuroleptic drugs to treat it, leading to increased risk of more prevalent tardive dyskinesia. Several studies have indicated that long-term neuroleptic use is associated with both cognitive deterioration and atrophy of the brain.
Did Reglan cause your Tardive Dyskinesia or Parkinson's Like Symptoms?
If you think you may have developed tardive dyskinesia or suffer from parkinson's like symptoms after taking Reglan / metoclopramide contact your doctor immediately. Please call us toll free 1-800-883-9858 to speak to us in person or fill out the form below and we will contact you back within 12-24 hours.