. . . antipsychotic drugs have been termed "neuroleptics," in that these drugs' actions imitate a neurological disease. - American Psychiatric Press, Textbook of Psychiatry (1988)Roberta had been treated for several years with the "miracle drugs," neuroleptics such as Thorazine, Haldol, Mellaril, and Prolixin. My medical evaluation described her condition:
Roberta is a grossly disfigured and severely disabled human being who can no longer control her body. She suffers from extreme writhing movements and spasms involving the face, head, neck, shoulders, limbs, extremities, torso, and back - nearly the entire body. She had difficulty standing, sitting, or lying down, and the difficulties worsen as she attempts to carry out voluntary actions. At one point she could not prevent her head from banging against nearby furniture. She could hold a cup to her lips only with great difficulty. Even her respiratory movements are seriously afflicted so that her speech comes out in grunts and gasps amid spasms of her respiratory muscles.Tardive Dyskinesia and Tardive Dementia
Roberta had an unusually severe case of tardive dyskinesia (TD), a disease frequently caused by the neuroleptics. The term "tardive" means late developing or delayed; "dyskinesia" means abnormal movement. Tardive dyskinesia is a movement disorder that can afflict any of the voluntary muscles, from the eyelids, tongue, larynx, and diaphragm to the neck, arms, legs, and torso.(1) On rare occasions it can occur after a few weeks or months, but usually it strikes the individual after six months to two years of treatment.
Any of the neuroleptics can cause tardive dyskinesia. The total dosage probably affects the likelihood of this happening, but the dose relationship is not easily demonstrated, and any amount must be considered dangerous. While some symptoms improve or even disappear after removal from the offending medications, most cases are permanent. There is no known treatment for tardive dyskinesia.
Often the start of disease goes unnoticed, because the drugs that cause it also tend to suppress the overt symptoms. Thus the disease percolates out of sight, finally breaking through with uncontrollable twitches, spasms, or writhing movements. Whenever possible, patients should try to stop the drugs periodically to check for abnormal movements.
Roberta also had tardive dementia, a global deterioration of her mind and mental faculties caused by the drugs. While tardive dyskinesia is a firmly established disease, tardive dementia remains more controversial within the profession, although evidence for its existence seems incontrovertible.
Had She Seen a Different Doctor ...
Roberta was a college student getting good grades, mostly A's, when she first became depressed and sought psychiatric help at the recommendation of her university health service. She was eighteen at the time, bright and well-motivated, and a very good candidate for psychotherapy. She was going through a sophomore-year identity crisis about dating men, succeeding in school, and planning a future. She could have thrived with a sensitive therapist who had an awareness of women's issues.
Instead of moral support and insight, her doctor gave her Haldol. Over the next four years, six different physicians watched her deteriorate neurologically without warning her or her family about tardive dyskinesia and without making the diagnosis, even when she was overtly twitching in her arms and legs. Instead they switched her from one neuroleptic to another, including Navane, Stelazine, and Thorazine. Eventually a rehabilitation psychologist became concerned enough to send her to a general physician, who made the diagnosis. By then she was permanently physically disabled, with a loss of 30 percent of her IQ.(2)
More "Mild" Cases of Tardive Dyskinesia
Most cases of tardive dyskinesia are labeled "minimal" or "mild," compared to "moderate" or "severe." But imagine how you would feel if your mild case of tardive dyskinesia made you stick out your tongue periodically in front of other people, or if you had to blink your eyes spasmodically or crane your neck oddly, or if your voice screeched a little out of control, while others were watching or listening.
An older woman came up to me after one of my lectures at a university. She was warm, friendly, and articulate; but what she was saying seemed undermined by the strange way she kept shrugging her right shoulder. Afterward, a friend of mine, perplexed, asked me, "What's up with her? She sounds rational, but she acts so strangely." I explained that the woman had been treated for years with neuroleptics. The hunching of her one shoulder was a mild case of tardive dyskinesia; but it was disfiguring enough to discredit and distract attention from what she was saying. That she was a former mental patient only made others more certain that her symptom was an expression of "mental illness."
You may recall passing someone on the street, perhaps an old and disheveled man, who seemed to be chewing a wad of gum. It looked ridiculous, the way he was chewing back and forth, and somehow you knew it wasn't normal, it wasn't just gum chewing. You figured it was a sign of craziness. The odds are that he had another mild case of tardive dyskinesia.
Or perhaps you saw a homeless man standing on a corner bouncing up and down from one foot to another like he had, as the old expression goes, "ants in his pants." That, too, was probably tardive dyskinesia, or a variant called tardive akathisia, which forces a person to move all the time, against his or her own will. It also can induce unbearable tension and anxiety.
The Lessons of Lethargic Encephalitis
Rather than treating a disease, the neuroleptics create a disease.
Delay and Deniker (chapter 3) were the first psychiatrists to experiment with the original neuroleptic, Thorazine, for psychiatric purposes in Paris in the early 1950s. They immediately noticed that small doses produced a neurological disease very similar to a special type of virulent flu virus that killed tens of thousands during and shortly after the First World War.
The type of flu mimicked by the drugs was called lethargic encephalitis (encephalitis lethargica), or von Economo's disease. "Lethargic" refers to a typical symptom of the disease, a sluggish or apathetic mental state. "Encephalitis" designates inflammation of the brain.
The similarity between the neuroleptic effect and lethargic encephalitis should have been a colossal warning against using the neuroleptics on human beings. Indeed, the viral disease and the drug-induced effects are so similar that to learn about lethargic encephalitis is to learn about the routine effects of the psychiatric medications. Yet the psychiatric literature has expurgated this important information so that most young psychiatrists are wholly unaware of it.
An esteemed text on the disease, Lethargic Encephalitis, was written by New York University professor of neurology Isador Abrahamson and published posthumously in 1935. Abrahamson's description of the effects of viral encephalitis are almost identical to the lobotomizing drug effect as described by Delay and Deniker and other neuroleptic pioneers:
Irritability both to internal and external stimuli diminishes, and the vital tone of the afflicted host lessens.... He may display neither conscious nor unconscious initiative . . . There is a complete lack of emotional expression . . . The face, waxen and corpselike, remains an impassive and inscrutable mask . . . In other words, sensory stimuli stream into the brain and the brain ignores them . . . [A]nd volition is practically suspended.Abrahamson uses a phrase to sum up the encephalitis victim's robotic condition - "psychomotor inertia." It, too, is almost identical to the phrase commonly used by psychiatrists to sum up the impact of the neuroleptics - "psychomotor retardation."
Similar Neurological Effects
After the mental lethargy that often heralded the onset of viral encephalitis, a variety of severe neurological symptoms manifested themselves as the disease progressed into its acute phase. These so closely parallel the various neurological reactions produced by neuroleptic medications that they can be discussed together.
The encephalitic patients would develop extremely painful, debilitating spasms of their muscles. This "dystonia" occasionally occurs early in the treatment of patients taking neuroleptic drugs.
The encephalitic patients developed bizarre forms of hyperactivity with an inner irritability that drives the person to move about. Sometimes it can reach extreme proportions of anxiety and anguish, with constant motion. This disorder, "akathisia," typically is found in up to half of the patients taking neuroleptics. A recent study by Joseph Lipinksi in the September 1989 Journal of Clinical Psychiatry found a rate of 71 percent for akathisia among a sample of 110 patients at Boston's McLean Hospital.
The victims of the virus often developed a variant of parkinsonism, including a tremor of the extremities, rigidity of movement and facial expression, a shuffling gait, and emotional flattening. Parkinsonlike signs occur in most patients treated with neuroleptics and in all patients given high doses. Many psychiatrists used to argue that the drugs could not have their maximum effect without producing some degree of parkinsonism. The muscles can become so rigid that the patient is unable to carry out aggressive actions or any other vigorous, spontaneous activity. This has been called the chemical straitjacket.
Neuroleptic Malignant Syndrome
Psychiatry has focused increasing attention on an especially dramatic toxic reaction to the neuroleptics occurring in a small percentage of patients treated with the drugs. Like the meltdown of a nuclear power
*These quotes are taken from chapter 2, "Mental Disturbances in Lethargic
plant, the drug reaction can get completely out of hand. The result,
neuroleptic malignant syndrome, is largely indistinguishable from an acute,
fulminating case of lethargic encephalitis.
Similar Permanent Neurological Effects
The most tragic similarity between lethargic encephalitis and the neuroleptics is their frequent production of permanent neurological disorders. After lethargic encephalitis, many patients seemed to recover fully. Then months or even many years afterward, many would unexpectedly begin to deteriorate neurologically. They might develop abnormal bodily movements, such as twitches, spasms, or snakelike movements. Most often they developed permanent parkinsonism. Some would deteriorate mentally into psychotic states or dementia.
The profession of psychiatry now agrees that the drug-induced neurological disorders do become permanent in a large percentage of patients. In addition, there is growing incontrovertible evidence that permanent psychosis and dementia also are frequent outcomes. Neuroleptics impact on the patient by causing a disease rather than by curing one.
They Knew from the Beginning
We don't have to speculate about whether Delay and Deniker anticipated the potential tragedy they were creating. In a reminiscence published in 1970 Deniker says that he knew from the beginning that the drugs could cause a worldwide epidemic of brain disease similar to lethargic encephalitis:
It was found that neuroleptics could experimentally reproduce almost all the symptoms of lethargic encephalitis. in fact, it would be possible to cause true encephalitis epidemics with the new drugs. Symptoms progressed from reversible somnolence to all types of dyskinesia and hyperkinesia, and finally to parkinsonism. The symptoms seemed reversible on interruption of the medication. (Italics added)Deniker also pointed out that the permanency of the damage could have been anticipated from the beginning:
Furthermore, it might have been feared that these drugs, whose actions compare with that of encephalitis and parkinsonism, might eventually induce irreversible secondary neurological syndromes. Such effects cannot be denied: it has been known for some years that permanent dyskinesias may occur. . . . (Italics added)The Degree of Risk
In 1980, eight years after the first definitive reviews and twenty-five years after the drugs first had been used, the American Psychiatric Association finally completed and published an official task force report on tardive dyskinesia. Its official summary for the rates of tardive dyskinesia in routine drug use over six months to two years are staggering: at least 10 to 20 percent of neuroleptic-treated patients would get more than minimal disease. In older people and longer-term use the rates escalated to at least 40 percent in hospitals and in clinics.
Data in the task force report show that the percentages of affected patients are in fact much higher than reported in their summary estimate. The task force examined one group of 506 patients with special care and tabulated the rates according to age. The rates surpassed 54 percent in men and 59 percent in women age sixty and over. Among more elderly women treated with the drugs, 66 percent suffered from tardive dyskinesia.
The task force cited some well-conducted studies showing tardive dyskinesia rates of 40 to 60 percent in clinics and in state hospitals.
Half or More of Long-Term Patients
As the APA figures suggest, half or more of long-term patients, as well as older patients, are likely to develop tardive dyskinesia. A few drug advocates have acknowledged this openly. In their 1986 Manual of Clinical Psychopharmacology, published by the American Psychiatric Press, Alan Schatzberg and Jonathan Cole note that tardive dyskinesia tends to develop at the rate of 3 to 4 percent per year and that "in chronically institutionalized psychotic patients, dyskinesia prevalence rates are often on the order of 50-60 percent" (p. 99). A 1981 pamphlet written by psychiatrist Robert Sovner and produced by the drug company Sandoz, observes that "up to 56%" of "chronically hospitalized patients" will develop tardive dyskinesia.
An Almost Certain Risk?
Some experts have begun to admit that nearly all long-term patients are likely to succumb to tardive dyskinesia. Guy Chouinard of Canada is one of the most experienced and best known researchers in the field. The June 1990 Clinical Psychiatry News reports on Chouinard's recent findings: "it appears that drug exposure of 15 years and more would lead to almost certain risk for tardive dyskinesia. " Unfortunately, many patients are told they must remain on neuroleptics for the rest of their lives, without being told about the huge and "almost certain" risk of developing a serious neurological disease.
A Court Verifies the Rates
While much of the psychiatric leadership continues to minimize and to misrepresent the risks of psychiatric drugs, the courts have become more convinced of the menace. In a supreme court case in Indiana in 1981, judge Evan Goodman gave the following opinion:
At the heart of this case is the virtually undisputed allegation that a person medicated with anti-psychotic drugs has a 50% risk of contracting tardive dyskinesia, a disease exemplified by twisting tongue movements, puffing cheeks, smacking of lips, sucking movements of the mouth, and face and body movements characterized by continuous rocking motions, tremors and bizarre postures, and other symptoms, and which at this time is incurable. (Italics added)What the Public Hears
Generally the profession tells the public and patients very little about tardive dyskinesia and greatly minimizes the risk. A fortunate exception is psychiatrist Jack Gorman in his book The Essential Guide to Psychiatric Drugs (1990). He warns the potential patient, "The risk of developing severe TD from antipsychotic drugs probably lies between 20% and 40%, but mild signs may appear in up to 70% of patients. Patients should be examined carefully by the doctor, at least every six months, for signs of TD" (p. 221).
If patients are taking these drugs, it is indeed imperative that the doctor carefully examine them frequently for signs of abnormal movements and that the patient and the family stay alert for them as well.
Confirming High Rates Among Older Patients
Recent investigations have confirmed the high rate of tardive dyskinesia in all age groups and have ruled out spontaneous dyskinesias of unknown origin as a major complicating factor. In Tardive Dyskinesia (1988), edited by Marion Wolf and Aron Mosnaim, a team led by Ramzy Yassa from McGill University found a rate of 41 percent among patients over age sixty-three after only twenty-four months of exposure to neuroleptics.
None of the nondrug controls in Yassa's study developed movement disorders during the test period of two years. Since the aged are the only group thought to be susceptible to an appreciable number of spontaneous motor disorders, this should lay to rest the argument that tardive dyskinesia rates are falsely inflated by nondrug movement disorders. As the September 1983 headline in Clinical Psychiatry News had already indicated, DYSKINESIA INCIDENCE HELD VERY LOW IN HEALTHY AGED POPULATION.
Confirming High Rates Among Children
Children frequently are given these medications in hospitals, facilities for delinquents, and, especially, institutions for the retarded. Typically they are used for the control of unwanted behaviors. This well-known fact was confirmed in a 1987 survey of practices in a children's state hospital by Benedetto Vitiello and others in the Journal of Clinical Psychiatry.
For a decade after the recognition of tardive dyskinesia, psychiatric experts supported the myth that children are less affected by tardive dyskinesia and that it is safer to give them the medications. Yet the review in my 1983 book Psychiatric Drugs: Hazards to the Brain made clear for probably the first time that rates among children are high and that children tend to suffer from especially incapacitating cases of the disease, often involving control of the torso, making it hard for them to sit, stand, or walk.
Fortunately, the myth about children being resistant to tardive dyskinesia seems to be dying. A study of drug-treated retarded children by C. Thomas Gualtieri and his colleagues, published in the April 1986 Archives of General Psychiatry, showed that 34 percent of the children developed tardive dyskinesia, the majority displaying moderate to severe symptoms. They stated, "One may conclude that TD, including severe and persistent TD, represents a substantial hazard to young retarded people treated with neuroleptic drugs." The risk, of course, is not limited to the retarded, but equally includes every child treated with these drugs. The study also showed that the children went through an especially agonizing period of withdrawal from the drugs, during which their mental anguish increased substantially.
Tardive Akathisia in Children and the Developmentally Disabled
Tardive akathisia - anxiety or nervousness and an uncontrollable drive to move the body - is a particularly insidious problem among children treated with neuroleptics. Especially in institutions for children and among people with mental retardation, the neuroleptics are given in order to control restlessness. It's easier to drug these persons than to provide more interesting and stimulating environments to occupy their energy. But when the drugs are administered for several months or more, there is increasing danger that they will produce tardive akathisia - a permanent need to move about, accompanied by sometimes dreadful anxiety. Thus the drugs create the very symptoms they are supposed to control, and the child ends up in a vicious circle, being given larger and larger doses in order to control the now-drug-induced disorder.
Akathisia, as already noted, is very common during neuroleptic drug treatment. How often it becomes permanent is more difficult to tell, but Gualtieri, one of the world's experts, estimates that tardive akathisia occurs in 13 percent or more of institutionalized developmentally disabled persons who are treated with neuroleptics .4 It is an irony of tragic proportions that we literally are creating hyperactive children and adults, saddled for the rest of their lives with sometimes excruciating inner turmoil and a drive to keep their bodies in motion all the time.
The Professional Reaction to Tardive Dyskinesia
For twenty years the profession simply failed to notice that a large percentage of its patients was twitching and writhing from the drugs. When the first highly visible reports came out in 1973 by George Crane in Science and by a joint committee of the American College of Neuropsychopharmacology and the Food and Drug Administration (FDA) in the Archives of General Psychiatry, the professional reaction was largely one of denial and rejection. The editor of the Archives, Daniel X. Freedman, appended an editorial to the report on tardive dyskinesia in which he warned the reader not to exaggerate the problem because it might impede congressional funding for beleaguered psychiatry. The late Nathan Kline, once the nation's most quoted drug specialist, said he'd never seen a case in his life, even though he conducted research in state mental hospitals where half or more of the patients are afflicted. Nor was Kline alone. Nearly every hospital and clinic psychiatrist in the world was at that time guilty of the same oversight.
The story of psychiatry's failure to take responsibility for injuring its patients is recounted in detail by Phil Brown and Steven Funk in "Tardive Dyskinesia: Barriers to the Professional Recognition of an Iatrogenic Disease" in the June 1986 Journal of Health and Social Behavior.(3) Brown and Funk cite George Crane's confirmation that "the majority of psychiatrists either ignored the existence of the problem or made futile attempts to prove that these motor abnormalities were clinically insignificant or unrelated to drug therapy." In a frightening revelation, Crane discloses that psychiatrists tended to increase their use of neuroleptics after he lectured them on their dangers.
Psychiatrists continue to be largely remiss about informing patients and their families about the dangers of tardive dyskinesia. As Brown and Funk observed in 1986, "psychiatrists do not, by and large, inform patients and their families adequately about the risks of TD." As we saw in Roberta's case, they can persistently fail even to recognize the disease they themselves have induced.(4)
Psychiatry's Special Concern
As the data on tardive dyskinesia piled up, psychiatry became more and more concerned - not for its patients, but for itself. On October 7, 1983, the official APA newspaper, Psychiatric News, declared in a headline: TD COURT CASES UNDERSCORE IMPORTANCE OF APA REPORT. It gave the bad news: two precedent-setting cases had been settled for $760,000 and $1 million. Another headline in the January 1984 issue of Clinical Psychiatry News shouts out the dreaded words: EXPECT A FLOOD OF TARDIVE DYSKINESIA MALPRACTICE SUITS. I know of no corresponding headline, such as BEWARE A FLOOD OF TARDIVE DYSKINESIA PATIENTS. It's the legal cases that worry psychiatrists.
In July 1985 the American Psychiatric Association followed up its task force report of five years earlier with an unprecedented letter to its nearly forty thousand members, which included nearly every psychiatrist in America. It repeated its warning that "at least 10-20% of patients in mental hospitals" and at least 40 percent of longer-term patients would get more than minimal signs of tardive dyskinesia. It also confirmed that children are at risk.
Why the unusual letter? One reason, at least, was self-serving: "We are further concerned about the apparent increase in litigation over tardive dyskinesia."
Since then, malpractice suits have escalated. TARDIVE DYSKINESIA LAWSUITS ON INCREASE warns a May 1989 headline in The Psychiatric Times. Expert Theodore van Putten estimated 400,000 to a million cases of the disease in the United States alone. Out-of-court settlements, the article says, were averaging $300,000, while jury awards were averaging $1 million.
NIMH Waters Down the Rates
As the tragedy of tardive dyskinesia unfolded, some doctors devoted themselves to making light of it. Dilip Jeste and Richard Jed Wyatt of NIMH and St. Elizabeths Hospital estimate a tardive dyskinesia rate of only 13 percent in their 1982 book Understanding and Treating Tardive Dyskinesia. While even a rate this high would be a medical catastrophe, the real figures are much higher. Jeste and Wyatt achieve their relatively low figures, first by assuming that one-quarter of reported cases are due to nondrug movement disorders (P. 32) and second by arbitrarily dropping out all cases in the literature except those labeled "moderate" and "severe" (P. 22). Without these manipulations of the data, which are buried in the text, their rate would be more than double the 13 percent.
In reality, the most careful studies have generated the highest rates. Stewart Tepper and Joanna Haas, in a December 1979 review in the Journal of Clinical Psychiatry, specifically focused on the better studies and found rates for tardive dyskinesia in the range of 24 to 56 percent for patients undergoing chronic neuroleptic treatment. Studies with low rates were typically very flawed. Tepper and Haas estimated that "close to 200,000 patients may develop tardive dyskinesia as a result of neuroleptics prescribed in 1978. " As an example of a well-conducted study, Psychiatrist Gregory Asnis and his colleagues, in 1977 in the American Journal of Psychiatry, reported using objective rating scales, more than one rater, and videotapes. They found that among outpatients in a New York City clinic, 43.4 percent suffered from tardive dyskinesia. Worse still, many had received the drugs for a year or less. One had been treated for only eight months.
The President of APA Tries to Deny the Rates
On the Oprah Winfrey TV talk show on August 17, 1987, 1 debated the president-elect of the American Psychiatric Association, psychiatrist Paul Fink. Shortly before I was introduced, psychiatric survivor Judi Chamberlin had warned the viewing audience about tardive dyskinesia. Now I further explained, "If individual people want to take drugs, that's their privilege. But they should know that long-term therapy in 50 percent of the cases is producing the neurological disease Judi mentioned."
Fink interrupted adamantly, "Fifty percent of the cases is an outrageous overstatement. Absolutely an outrageous overstatement."
I corrected him, "The Psychiatric Association's Task Force on Tardive Dyskinesia said - - "
Fink began shouting and interrupting again, "Never said 50 percent."
"It says 40 percent get more than minimal disease," I said, completing my sentence.
"Never said!" he shouted again. "Never says 40 percent."
There it was. The president-elect of the American Psychiatric Association could not possibly be ignorant of the data from the APA report, especially since the 40 percent figure had been published repeatedly in the association's books, journals, newspapers, and even an official letter to the membership two years earlier.
At the next break for advertising, I retrieved from my briefcase my copy of the official APA task force report, Tardive Dyskinesia. When the show resumed, I read aloud the statement, quoted earlier in this chapter, that at least 40 percent of long-term patients will be afflicted with tardive dyskinesia.
Newly Recognized Manifestations of Permanent Neurological Damage
There's increasing recognition of variations on tardive dyskinesia, including tardive dystonia, with recurrent muscle spasms that are agonizing to the patient, and tardive akathisia, described earlier in this chapter. As with the other tardive disorders, there are no known treatments for them.
Cases are appearing of patients permanently unable to control their water intake, leading to water intoxication, as well as cases of the chronic disability of temperature control mechanisms, leading to heat stroke. The growing array of problems stimulated a story in the November 1987 issue of Clinical Psychiatry News with the headline DYSKINESIA 'TIP OF ICEBERG' OF NEUROLEPTIC SYNDROMES.
Beneath the "tip of the iceberg" of neuroleptic syndromes lurks something far more threatening.
Deterioration of the Mind from Neuroleptic Treatment
When I first began to review the extensive literature about tardive dyskinesia, all of the psychiatric textbooks assumed that it was a disease affecting muscular control without imperiling the mind. Intuitively, and from what I knew scientifically of the integration of brain and mind, it seemed implausible to ruin the motor control systems without harming the mind as well. My research resulted in a lengthy overview on permanent mental dysfunction from the neuroleptics, published as a chapter entitled "Lobotomy, Dementia, and Psychosis Produced by the Major Tranquilizers" in my 1983 medical book Psychiatric Drugs: Hazards to the Brain. Seven years later I followed this with an updated, still more detailed review, "Brain Damage, Dementia and Persistent Cognitive Dysfunction Associated with Neuroleptic Drugs: Evidence, Etiology, and Implications," in the Journal of Mind and Behavior.
Briefly, the basal ganglia are most clearly damaged during the production of tardive dyskinesia by the neuroleptics. Pathological findings in Parkinson's disease and Huntington's chorea indicate that they influence control and coordination of the muscles. But the basal ganglia also are intimately connected to the higher mental centers, and diseases affecting the region ultimately impair the mind. Tardive dyskinesia is caused by permanent hyper-reactivity in the dopamine neurotransmitter system in this area. But dopamine is also the main neurotransmitter ascending into the emotion-regulating limbic system and frontal lobes. The lobotomy effect results from the action of the drugs on these nerve pathways. When this region also becomes permanently hyper-reactive in response to the neuroleptics, as we know it does, it would make damage to the higher brain and mind inevitable.
The clinical literature confirmed my initial suspicions and my surmise that permanent damage to the highest mental centers was inevitable. ne initial studies of tardive dyskinesia showed that many and sometimes all patients also were suffering from serious mental dysfunction, including dementia. These threatening revelations were literally in small print and in charts, and seldom were commented on.
1. The description of tardive dyskinesia may seem familiar to people who have seen the recent movie Awakenings. When the main character, Leonard, deteriorates while taking large doses of L-Dopa, his extreme and disabling involuntary movements are identical to a very severe case of tardive dyskinesia.
2. I've seen several cases where multiple physicians have continued medication and failed to make the proper diagnosis. It appears as if the second and third doctors too often simply go along with the treatment, or else actually try to cover for the earlier doctor's mistakes. In some cases the denial of the Iatrogenic disease becomes grossly negligent. Patients have been seen in emergency rooms and have been psychiatrically hospitalized for days or weeks without anyone on the medical or nursing staff noting the existence of gross tremors, twitches, and other abnormal movements. Even physicians doing physical examinations may somehow neglect to notice or record the telltale signs of drug-induced neurological disease.
3. Brown and Funk point out that at the time of thorazine's introduction in the United States, its toxic effects and potential for causing damage were almost wholly ignored in the rush to use it as an agent of control in the state mental hospitals. Although it had been tested on only 104 patients in this country, Smith Kline and French promoted Thorazine so successfully that within eight months in 1954 the astounding number of two million Americans had been Placed on the medication, nearly all of them involuntary inmates in state mental hospitals.
4. In 1987 Peter Weiden and his colleagues from the Cornell Medical Center published a study in the American Journal of Psychiatry aptly entitled "Clinical Nonrecognition of Neuroleptic Induced Movement Disorders: A Cautionary Study." A July 1988 report in Clinical Psychiatry News confirms that psychiatrists continue to underdiagnose the disease. Using the standard of mild but definite symptoms, independent researchers in one study found a 48-percent rate of tardive dyskinesia; but the treating psychiatrists had noted signs of the disease in only 12 percent of the same group of patients. The treating doctors were especially prone to miss more subtle signs, such as difficulties in breathing and swallowing. The latter can be life-threatening. But they also missed more obvious signs, such as movements of the arms and legs.
Peter Breggin's Home Site - Peter R. Breggin, M.D. founded The International Center for the Study of Psychiatry and Psychology (ICSPP) as a nonprofit research and educational network concerned with the impact of mental health theory and practices upon individual well-being, personal freedom, and family and community values. For 25 years ICSPP has been informing the professions, media and the public about the potential dangers of drugs, electroshock, psychosurgery, and the biological theories of psychiatry.
Suggested Reading:Brain-Disabling Treatments in Psychiatry : Drugs, Electroshock, and the Role of the FDA Today! by Peter R. Breggin, M.D.
The Manufacture of Madness : A Comparative Study of the Inquisition and the Mental Health Movements by Thomas S. Szasz, M.D., Professor
Law, Liberty, and Psychiatry : An Inquiry into the Social Uses of Mental Health Practices by Thomas S. Szasz, M.D., Professor
The Limits of Biological Treatments for Psychological Distress by Seymour Fisher and Roger P. Greenberg
Psychiatric Drugs: Hazards to the Brain by Peter R. Breggin, M.D.
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