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Dyskinesia, drug induced Definition
Dyskinesia, drug induced generally refers to the symptom that is caused by the high-dose or long term usage of the drug calleddopamine antagonists, which are usually used as antipsychotics medications and antiemetic metoclopramide. Such neuroleptic drugs are generally used to be prescribed to treat a number of different types of psychiatric disorders. Other forms of dopamine antagonists that are known to cause tardive dyskinesia are drugs used for the treat cases of gastrointestinal disorders along with some neurological disorders. Majority of the drugs that are not actually intended to affect the dopamine, such as the antidepressants, may be also the main cause of tardive dyskinesia. While there are newer atypical antipsychotics available in the market today such as olanzapine and risperidone that may initially appear to have lesser dystonic ill-effects, only clozapine has been proven to have a signioficantly lower risk of complications such as tardive dyskinesia in comparison to the older antipsychotics.
Dyskinesia, drug induced Treatment
As far as medical treatment available for iatrogenic tardive dyskinesia is concerned, the neuroleptic drugs should be gradually withdrawn for a period of at least 3-6 months to be able to see if this discontinuation of the medication will resolve the issue, but the main problem may have failed to improve. In such situation, it would be more practical and sensible to provide trial to the patient on tetrabenazine 25-50 mg/8h PO.
Dyskinesia, drug induced Causes
Despite tardive dyskinesia been known to exist for over more than 50 years, its etiology still largely remains poorly understood mainly due to the rather limited research that were conducted on the side effects of this psychiatric drug. The main underlying cause of the tardive dyskinesia have been known to appear to be related to certain damage to the patient's internal system which is believed to use and process the neurotransmitter dopamine. Among the most compelling lines of evidences that suggest the tardive dyskinesia may often result primarily from the neuroleptic-induced dopamine supersensitivity in the body's nigrostrial pathway, along with the D2 dopamine receptor being said to be the most affected. Neuroleptics typically act firstly on the dopamine system, and then the older neuroleptics, which have a considerably greater affinity for the site of the D2 binding, are to be associated with the high and intensified risk for tardive dyskinesia.
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