Several million people are treated with neuroleptic medications (major tranquilizers or antipsychotics) in North America each year. A large percentage of these patients develop a chronic neurologic disorder - tardive dyskinesia - characterized by abnormal movements of the voluntary muscles. Most cases are permanent and there is no known treatment. Evidence has been accumulating that the neuroleptics also cause damage to the highest centers of the brain, producing chronic mental dysfunction, tardive dementia and tardive psychosis. These drug effects may be considered a mental equivalent of tardive dyskinesia. Relevant data are derived from human autopsies, brain imaging (CT, MRI and PET scans), neuropsychological tests, and clinical research. That the neuroleptics can damage higher brain centers is confirmed by their known neurotoxicity and neurophysiological impact, animal autopsies, and a comparison to diseases that mimic neuroleptic effects, such as Huntington's chorea and lethargic encephalitis. Patients and the public should be informed of the danger of both tardive dyskinesia and tardive dementia. The mental health professions should severely limit the use of neuroleptics and develop safer and better alternatives to these dangerous substances.
The neuroleptics, also known as major tranquilizers or antipsychotics, are among the most widely used drugs in psychiatry. In the United States and Canada alone, millions of adults and children receive these medications in general hospitals, private and public mental hospitals, board and care homes, institutions for the developmentally disabled, nursing homes, prisons, clinics and private practice. While the medications are most often advocated for patients diagnosed as schizophrenic or manic, they are in fact widely used as a method of social control. In many institutions, most of the inmates will be receiving them (Breggin, 1983).
It is now widely recognized that the neuroleptics frequently produce a largely irreversible neurological disease, tardive dyskinesia, in a significant number of patients. New evidence is accumulating that the same drugs can also cause persistent damage or dysfunction to the highest centers of the brain, resulting in irreversible intellectual and emotional impairments, including tardive dementia and tardive psychosis. These effects may be viewed as the mental equivalent to tardive dyskinesia.
Although concerns about neuroleptic-induced damage to the highest centers of the brain have been voiced for more than a decade (Marsden, 1976), it was not until 1983 that the subject was analyzed in depth (Breggin, 1983, pp. 110-146). Since then, a considerable amount of relevant evidence has been published. In the first part of this article, I will review evidence of cognitive deficits, dementia and atrophy in neuroleptic-treated patients. In the second part I will explore the etiology.
The term dementia will be used as defined in the Diagnostic and Statistical Manual of Mental Disorders (third edition, revised, American Psychiatric Association [APA], 1987) [DSM-III-R]: "The essential feature of Dementia is impairment in short- and long-term memory, associated with impairment in abstract thinking, impaired judgment, other disturbances of higher cortical function, or personality change" (p. 103). The DSM-III-R states "As in all Organic Mental Syndromes, an underlying causative organic factor is always assumed" (p. 103). Acute drug-induced disorders that can cause brain damage and impair mental function, such as neuroleptic malignant syndrome or toxic psychoses, will not be considered in this article which deals with more gradually evolving persistent brain damage and dysfunction associated with chronic exposure to neuroleptics.
Reliance upon the neuroleptics for the treatment of acute schizophrenia is almost universal in psychiatry and most psychiatrists use them as the first line of treatment in these cases (see any recent textbook of psychiatry, for example, Nicholi, 1988; or Talbott, Hales, and Yudofsky, 1988). Occasional criticism of their use has been made (Breggin, 1983; Cohen and Cohen, 1986; Mosher and Burti, 1989). I have documented that the neuroleptics have no specific ameliorative effect on any mental disorder and that they are non-specific brain-disabling agents that perform a chemical lobotomy, in part through disruption of dopamine neurotransmission in the limbic and frontal lobe pathways (Breggin, 1983). The drugs do not cure a disorder but instead flatten the emotions, produce disinterest or apathy, and enforce docility. In a controlled study, Mosher and Burti (1989) demonstrated that almost all patients undergoing their first schizophrenic episode can be treated more successfully without neuroleptics than with them.
Terms like schizophrenia and schizophreniform, based on DSM-III or DSM- III-R, are used largely without reservation in most of the studies reviewed, and I have adopted this language for convenience in communicating. Several fundamental assumptions behind this classification - including the disease model - create a bias toward believing that a supposedly medical disease, schizophrenia, has caused the physical disorders found in the brains of these patients. This built-in bias should not distract us from properly evaluating the etiology of the damage. In my own opinion, schizophrenia is neither genetic nor physical in origin (Breggin, in press). The lay term, madness, is more appropriate to this psychosocial phenomenon. I have suggested alternative explanations elsewhere (Breggin, 1980d, in press).