Mental Health: Comes With FREE Tardive Dyskinesia

22 of the 23 Psychiatric Poisons in our FDA Adverse Reaction section feature Tardive Dyskinesia as an FDA reported Adverse Reaction with each Drug Individually identified as 'The Primary Suspect Drug' responsible for that Adverse Reaction

Abilify: Tardive Dyskinesia
Adderall: Tardive Dyskinesia
Celexa: Tardive Dyskinesia
Clozapine: Tardive Dyskinesia
Cymbalta: Tardive Dyskinesia
Depakote: Tardive Dyskinesia
Effexor: Tardive Dyskinesia
Geodon: Tardive Dyskinesia
Klonopin: Tardive Dyskinesia
Lamactil: Tardive Dyskinesia
Lexapro: Tardive Dyskinesia
Neurontin: Tardive Dyskinesia
Paxil: Tardive Dyskinesia
Prozac: Tardive Dyskinesia
Risperdal: Tardive Dyskinesia
Ritalin/Concerta: Tardive Dyskinesia
Seroquel: Tardive Dyskinesia
Strattera: Tardive Dyskinesia
Tegretol: Chorea
Wellbutrin: Tardive Dyskinesia
Xanax: Tardive Dyskinesia
Zoloft: Tardive Dyskinesia
Zyprexa: Tardive Dyskinesia

Wiki has:

Cause

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. 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 individual differences 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.

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