C. Antipsychotics and Progressive Brain Dysfunction

 

There are three main dopaminergic pathways in the brain. One involves the basal ganglia, which controls the initiation of motor movements. The second involves the limbic system, which is the area of the brain that helps us mount emotional responses to the world. The third is in the frontal lobes, which is the part of the brain that gives rise to self-consciousness.

 

Antipsychotics work by blocking dopamine receptors along these three pathways, and over the long-term, these pathways become increasingly dysfunctional (as least in a high percentage of patients.) The dysfunction in the basal ganglia leads to tardive dyskinesia. The dysfunction in the limbic system and the frontal lobes may lead to tardive psychosis and tardive dementia.

 

With the old standard neuroleptics, tardive dyskinesia was found to appear in five percent of patients within one year of treatment, with the percentage so afflicted increasing an additional five percent with each additional year of exposure. It was hoped that the new atypicals like Zyprexa and Risperidone would not cause as many tardive problems as the old drugs like Thorazine and Haldol, but there is now evidence suggesting that the new drugs may cause this progressive brain dysfunction with the same frequency.

 

Researchers have compared tardive dyskinesia to “known neurological diseases, such as Huntington’s disease, dystonia musculorum deformans, and postencephalitic brain damage.” Here are a handful of the studies that have documented this drug-caused brain dysfunction.

 

 

 

 

 

 

 

Twenty percent of patients on atypicals developed tardive dyskinesia in less than five years, a rate similar to that with standard neuroleptics. Severe TD may even more of a problem with the atypicals than with the standard neuroleptics.

 

 

A good review of the research literature documenting the many pathological effects of antipsychotic drugs.