sis" and in the next reveal that "the tardive dyskinesia patients at our hospital tend to be severely impaired by their psychosis and do not complain about their neurological disability." If antipsychotic drugs are so effective in combating psychosis, how can it be that a person could be afflicted with tardive dyskinesia and not even have sufficient awareness to issue complaint, to even know there is something wrong with his body? Obviously, there is a rather glaring inconsistency here. The various attempts to treat tardive dyskinesia have included the use of Librium, Valium, Lithium, Barbituates, and brain surgery." Reserpine, which can cause tardive dyskinesia and may induce a suicidal depression, has also been tried. One of the methods employed in the treatment of tardive dyskinesia and assuredly the most paradoxical and inexplicable and therefore the most likely to be adoped by psychiatry is increasing the dose of the drug which caused the condition in the first place. At least as far back as 1964 it was stated this method would produce improvement in the symptoms of TD" (though no improvement in the actual disease.) Observations of this sort led to "scientific" theorizing of this kind:

***72

*** It would thus appear possible that the most potent dyskinesia-producing phenothiazines might have the most potent dyskinesia-suppressing efficacy In psychiatry that which causes disease is that which improves it, that which makes one worse makes one better, and that which makes one ill makes one well. It is a treatment ideology that is completely upside down and absolutely devoid of

common sense.

While it is no doubt true that the symptoms of tardive dyskinesia can be suppressed with a larger amount of chlorpromazine (Thorazine) or haloperidol (Haldol) or whatever antipsychotic drug, doesn't this then place the patient into a vicious circle of never being free from drugs, of always needing a "fix"? Most people would consider the deliberate creation of such a situation unconscionable but there are psychiatrists who are willing to chance it and who consider the induction of tardive dyskinesia a therapeutic inevitability:

It is well known, of course, that certain few patients respond to no other form of treatment, even ECT, and in these patients, if chronic large dose neuroleptic therapy is required to give them relief from their psychosis then the induction of a neurological condition-even an irreversible one-cannot, in all respects, be considered a therapeutic failure.73

74

Aside from the fact that no acceptable form of treatment has been developed to even symptomatically treat tardive dyskinesia, there is another factor which makes handling of it still more complicated. Tardive dyskinesia and parkinsonism may coexist. An individual may be afflicted with both at the same time. He may suffer uncontrollable movements of the mouth, tongue, nose, lips, and jaw, and simultaneously be subjected to the rigidity of parkinsonism. Treatment for one condition exacerbates the other: 75 antiparkinson drugs make tardive dyskinesia worse and drugs used to suppress tardive dyskinesia make parkinsonism worse. Thus, the individual is ironically caught betwixt and between two physician-induced diseases-diseases created by the doctor through his use of drugs.

Perhaps, the greatest irony associated with tardive dyskinesia is not that it is an overwhelming problem born of a solution (mind-altering drugs) to a lesser problem (irrational behavior), nor even the fact that it is an iatrogenic disorder, but that a person suffering from it may be so disfigured and even crippled that he may indefinitely have to spend his life in the confines of a hospital when ostensibly the purpose of his drug therapy was to achieve the very opposite:

Few families, friends or neighbors would tolerate for long witnessing the abnormal movements. Hence, patients with persistent dyskinesia may have to remain in the hospital because of a complication of the therapy designed to get them out of [the] hospital.76

Given the nature of tardive dyskinesia it is relevant to inquire as to how the victims of it react. One would expect an individual maimed with this physicianinduced disease to be mentally tormented. It is rather shocking how often this is not the case. Psychiatrists claim this situation is so because the person's schizophrenia doesn't allow him to perceive what his body is doing-he is, in effect, "protected"

70 Ibid., p. 495-6.

71 Ibid., p. 494.

72 Ibid., p. 494.

73 William E. Fann et al., "On the Coexistence of Parkinsonism and Tardive Dyskinesia, "Diseases of the Nervous System, v. 35, p. 326, 1974.

74 William E. Fann et al., "Drug Induces Parkinsonism A Re-evaluation," Diseases of the Nervous System, v. 36, p. 92, 1975.

75 Ibid., p. 92.

76

Ayd, "Persistent Dyskinesia: a Neurological Complication of Major Tranquilizers," Medical Science, v. 36, p. 92, 1975

from tardive dyskinesia by his mental aberration. In other words, the person's emotional difficulties have in no way been affected by antipsychotic drugs. He is as out of communication with his environment and his own body as ever. This explanation is actually quite startling because it at once provides incontestable argument as to the worthlessness of antipsychotic medication. If an individual is administered a drug like Thorazine and the final product of such treatment is a person disabled by tardive dyskinesia and unaware that part of his body are twisting and contorting, then isn't he at least as worse off as before drug treatment? Yes. Before treatment he didn't suffer the ravages of tardive dyskinesia nor the emotional or psychic trauma caused by mind-altering drugs. Now he must endure both, with his original problems completely unhandled and probably worse.

It is difficult to believe that the apathy-inducing, chemical-lobotomizing effects of antipsychotic drugs aren't also a major factor in the person himself being kind of "not there," sort of "elsewhere" as his body goes through all manner of bizarre movement.

At a workshop sponsored by the National Institute of Mental Health in 1968, Dr. Rudolf Degkwitz commented on his experience with one group of tardive dyskinesia victims:

"*** We asked the 273 patients referred to earlier whether they experienced any discomfort. Only 20% were aware of the presence of motor abnormalities; the majority said that it was a habit or something to this effect. However, in nine cases, continuous rocking and intense grimacing appeared to cause considerable distress." 77

* *

78

Dr. Frank Ayd, in a comprehensive description of tardive dyskinesia written in 1967, stated that victims usually don't suffer any "subjective distress": “* Since they [the abnormal movements] seldom cause any subjective distress, many patients seem unaware of their existence. A few patients are tormented by this syndrome." Dr. George Paulson of the Department of Medicine at the Ohio State University wrote in a journal article published in 1975 that parkinsonism, akathisia, and tardive dyskinesia (see pages 24, 27, and 5 for definitions) aren't things about which the person usually complains:

"What significance does the parkinsonism, akathisia, or even TD have for the patient? The patients rarely complain about the movements, though they complain about slowing due to a drug-induced akinesia [abnormal absence of movement]." "9 And an article appearing in the British Journal of Psychiatry in 1969 detailed the fact that not even crippling choreiform movements necessarily capture the person's attention:

*

Continuously occurring irregular, jerky movements of the head, neck, trunk and limbs were so violent that she was unable to walk, stand or feed herself. Respiration was jerky and irregular, but bouts of acute distress with cyanosis (see page 22 for definition) were not seen. The abnormal movements of the face, tongue and jaw had also increased, but to a smaller degree. Tremor, rigidity, and other signs of parkinsonism had disappeared.

'At this time, and throughout the whole period of observation, her affect [emotion, feeling] was markedly flat, she never complained, and seemed indifferent to her state." 80

There is an element to the history of tardive dyskinesia that remains a mystery. The disorder was initially observed in 1957,81 described comprehensively by the mid1960's, and confirmed as a major public health hazard by the late 1960's. Yet it was not until May, 1973 that the Food and Drug Administration issued any kind of warning on TD. Coincident with this issuance the pharmaceutical industry finally began to acknowledge its existence and to provide warnings of its risk in the Physicians' Desk Reference, the source of drug information to which most doctors

turn.

It is strongly arguable that tardive dyskinesia should have been recognized as a threat to public health by the mid-1960's, for by that time it had been well delineated in the medical literature. An article appearing in Psychopharmacologia in 1960 addressed itself to a syndrome described as sometimes irreversible:

77 "Psychotropic Drugs and Dysfunctions of the Basal Ganglia-A Multidisciplinary Workshop," edited by George E. Crane and Russell Gardner, p. 30, 1968.

78 Ayd, "Persistent Dyskinesia: A Neurological Complication of Major Tranquilizers," Medical Science, v. 18, p. 34.

79 Paulson, "Tardive Dyskinesia,” p. 78.

80P. F. Kennedy, "Chorea and Phenothiazines," British Journal of Psychiatry, V. 115, P. 103, 1969.

81 George E. Crane, "Dyskinesia and Neuroleptics," Archives of General Psychiatry, v. 19, p. 700, December, 1968.

S. G. Carruthers, "Persistent Tardive Dyskinesia," British Medical Journal, v. 3, p. 572, 1971.

"The neurological symptoms which we have observed being irreversible in some cases is a syndrome. . . consisting of incessant involuntary munching and masticating movements of the jaw during which the tongue is protruded at short intervals with vigorous grimaces of the lips. . . . In the most serious cases there are also rocking and torsionary body movements and incessant triping and shuffling movements so that the patient can not stand still." 82

It went on to state that elderly persons seemed to have a particular vulnerability to this disorder:

"It should be noted that the patients in which the dyskinetic syndrome occurs are rather old, the average age being 66, and among the younger patients several have an organic brain disease. Therefore it may be presumed that the dyskinetic syndrome occurs most easily in elder persons and in persons with organic brain lesions." 83

In August, 1964 three English doctors published an article in the Proceedings of the Royal Society of Medicine in which they included serial photographs depicting the abnormal mouth, tongue, and jaw movements of dyskinesia, and in which they stressed the urgency of bringing attention to the disorder and correcting the erroneous impression that phenothiazines could be administered indefinitely without consequence of irreversible harm:

"Once this syndrome is generally recognized we suspect a spate of cases will come to light, especially since ten years have now elapsed since phenothiazines were introduced into psychiatry and many will have received the drug long enough to manifest these effects. It seems to us therefore an urgent matter to draw attention to this unfortunate, distressing and seemingly irreversible complication of these widely used drugs, the more so since the advice that they should, and safely may be continued indefinitely is still given in the literature and not only in that issuing from pharmaceutical firms."84

Unfortunately, only three months later a comment in the Canadian Medical Association Journal attempted to discount the value of the above paper, characterizing it as giving "rise to somewhat unnecessary alarm in the popular press." 85 It indicated that the cases discussed all suffered brain damage and suggested that this element threw into doubt whether or not the movements observed were solely the result of phenothiazine medication. The brain damage that these patients suffered, however, was in the majority of cases the product of psychiatric treatment, namely, leucotomy, electroconvulsive shock, and insulin coma treatment.86

In this editorial the Canadian Medical Association concluded that persistent dyskinesia was one of the "side effects" of phenothiazine treatment that had to be accepted in treating schizophrenia, for they claimed there was nothing else effective.

One month later in December, 1964 the British Medical Journal offered a more reasoned evaluation:

"These reports suggest that prolonged administration of phenothiazine derivatives may cause not only transitory and functional changes but also permanent and therefore presumably structural changes in the nervous system. The risk seems to be greatly increased when the patient's brain is damaged or diseased. It is clearly important to be on the look-out for this syndrome. While no one doubts the value of phenothiazine derivatives, it is essential to know the possible risks entailed in order to weigh them against the probable benefits." 87

Only one more month past before, in January 1965, the American Medical Association addressed itself to the subject of irreversible dyskinesia in its own journal, JAMA. On this matter and on the subject of irreversible purple coloration of the skin occurring with chloropromazine intake, this highly influential organization called for only "physician awareness" of the problem:

"The occurrence of such rare sequelae should not detract from the general usefulness of the phenothiazines in the management of the schizophrenic illnesses. Nevertheless, it is important that physicians treating patients with high and prolonged

82 L. Uhrbrand et al., “Reversible and Irreversible Dyskinesia after Treatment with Perphenazine, Chlorpromazine, Reserpine, and Electroconvulsive Therapy", Psychopharmacologia, v. 1, p. 408.

83 Ibid., p. 417.

Richard Hunter et al., "An Apparently Irreversible Syndrome of Abnormal Movements Following Phenothiazine Medication, "Proceedings of the Royal Society of Medicine, v. 57, p. 762, 1964.

85 Canadian Medical Association Journal, v. 91, p. 1081, November 14, 1964.

86 Richard Hunter et al., op. cit., p. 759.

87 British Medical Journal, v. 2, p. 1412, 1964.

dosages of phenothiazine drugs be aware of the possibility of permanent sequelae following use of these agents." 88

In April, 1966 a paper appeared in the Archives of Neurology that described fives cases of persistent dyskinesia and which concluded that drug advertising of the time was not altogether conducive to the practice of good medicine:

"The risks of treatment, pharmacological, surgical, or whatever, are always with us. Current drug advertising makes implicit or even explicit suggestions that the phenothiazines are safe guides to serenity, entailing "little risk of untoward effects," and they are recommended for "agitation, tension, apprehension or anxiety (moderate to severe.)" While such statements are ordinarily phrased carefully, they do not always appear to serve the best interests of responsible medical practice." "

In June, 1966 the International Drug Therapy Newsletter carried a 34-point description of persistent dyskinesia, fully detailing all of its main features. By this time persistent or tardive dyskinesia had been thoroughly described in the medical literature in many articles and its existence as a unique and distinguishable nosological entity and its relationship to the intake of antipsychotic drugs was beyond question, yet nearly seven years were to pass before the FDA or the pharmaceutical industry issued warning of its risk.

Probably the one person most responsible for attacking the issue of tardive dyskinesia foursquare and sounding the alarm on it was Dr. George Crane. Crane is not a so-called antipsychiatry psychiatrist nor is he blanketly opposed to the use of mind-altering drugs. In 1967 when he convened the first major conference on tardive dyskinesia he was with the Psychopharmacology Research Branch of the National Institute of Mental Health. In spite of his "establishment" credentials he was for some time, in the words of Dr. Nathan Kline, "a lone voice crying in the wilderness."

Kline himself was a lone voice of sorts. During the period of greatest controversy over TD he most represented the position which sought to minimize the frequency and hazards of it. In 1968, in a flagrantly gross understatement of the occurrence of tardive dyskinesia, he wrote:

66* * *

Since there are less than two dozen reported cases in non-brain-damaged patients among 100 million estimated users the finding is interesting but not of great clinical significance." 90

And of Dr. Crane he has said:

66* *

* He's got a hobby horse which he's riding on the King's highway, which is all right as long as he doesn't hog the road." 91

In January, 1967 Crane committed the rather graceless act of "hogging the road" and gathered together at the Missouri Institute of Psychiatry in St. Louis the participants of the First Workshop on Tardive Dyskinesia.

One of the subjects discussed at this symposium was whether or not tardive dyskinesia was a major public health problem, and, if so, why it hadn't attracted attention before. It was claimed that failing to recognize the syndrome as something new and unique stemmed from its similarity to the persistent movements sometimes seen among mental hospital residents, movements that occur independent of any neuromuscular disorder. Elderly persons suffering from a condition known as senile chorea are also subject to uncontrollable movements which supposedly are confusable with TD.

It is true that abnormal movements bearing semblance to tardive dyskinesia have occurred among institutionalized mental patients and that such occurrence in some has been legitimate basis for confusion. This situation however has not been the case in most afflicted with tardive dyskinesia. Dr. George Crane expressed this fact quite clearly back in 1968:

"It is rather easy, I think, to distinguish what we call tardive dyskinesia from the stereotypes, [naturally occurring abnormal movements seen among schizophrenic patients] mannerisms, and rituals which we observe in schizophrenia and other psychoses although there may be some problem in making a differential diagnosis in borderline cases."92

Furthermore, after phenothiazine medication had been in widespread use for a period of time the percent of patients manifesting persistent abnormal movements dramatically increased. According to a survey done in 1955 at the Greystone State

88

8 JAMA, v. 191, No. 4, p. 158, 1965.

89 William R. Schmidt et al., "Persistent Dyskinesias Following Phenothiazine Therapy," Archives of Neurology, v. 14, p. 376.

90 Nathan S. Kline, "On the Rarity of Irreversible Oral Dyskinesias Following Phenothiazines," American Journal of Psychiatry, v. 124, p. 51, Feb., 1968, Supplement.

91 Tom Huth, "Mind Medicine's Side-Effects: Are the Risks Worth the Cure," Washington Post, Section B, p. 3, April 9, 1972.

92 George E. Crane and Russell Gardner, op. cit., p. 60.

Hospital in New Jersey, prior to the implementation of these drugs, those patients observed to have abnormal movements of whatever type was less than 1 percent.93 Dr. George Paulson, a participant at the workshop, was one of those who pointed out this increase and that failure to notice tardive dyskinesia previously made no case for its nonexistence:

"But the thing that has disturbed me most, and I am a believer that this is drugeffect, is that if you go spend time on the back wards, you see dozens of patients with these movements, and I don't remember having seen such a prevalence several years ago

*

* * *

can

"Also, I am undisturbed that we never noticed these movements until lately. Certainly, a medical student who studies Parkinsonism for the first time usually fails to notice the characteristic facies [faces] until it is pointed out to him we tell ourselves that there is no such thing as a permanent drug effect? If we do this, we must remember that not only Dr. Crane, but numerous responsible people in Europe have made identical observations. In our country, very little has been written on the syndrome." "'94

Interestingly, he also mentioned something which has long been one of the fundamental operating principles of psychiatry and which all the participants perhaps showed a certain reticence to bring up:

"This suggestion, that brain damage furthers therapy, is an old argument that has not come up today. It does seem true that electric shock, for instance, works better if the patient gets some confusion."95

Thus it seems, contrary to what has been asserted about convulsions, deliria, fever, malaria, parkinsonism, and other iatrogenic disorders, tardive dyskinesia is not mentally therapeutic.

Almost two years later in October, 1968 the National Institute of Mental Health sponsored another national workshop on tardive dyskinesia. Dr. George Crane opened the conference with these remarks:

66#

* Unless new and revolutionary discoveries are made in psychiatry, the duration of drug therapy for major psychiatric diseases will soon be measured in decades rather than years * * *. Tardive dyskinesia was practically unknown only a few years ago, but at present, manifestations consistent with this syndrome can be earily recognized in large numbers of long-term hospital populations. . . . In the early days of psychopharmacology, clinicians expressed concern about the possibility of neuroleptics 96 causing lasting effects on the central nervous system, but it was only in the late fifties that German and French authors identified a new syndrome that persisted after the withdrawal of phenothiazines '[Emphasis is added] 97 And Dr. Rudolp Degkwitz closed it with these:

66# * * many such cases can be seen if one takes the trouble of walking through the wards of mental hospitals. I feel that we should revise our therapeutic approach with drugs as the risk seems to be considerable. Twenty to 25 percent of the patients are afflicted by this disorder according to our observations; the disorder may last for many years or perhaps indefinitely in the more severe cases. Even if symptoms persist only for months of a few years in the milder cases, the problem still is of considerable clinical importance."

198

So it was, that by the end of 1968 the existence and gravity of tardive dyskinesia as a public health problem of alarming magnitude had been incontestably established. Hundreds of cases had been described in the medical literature and two national symposia convened under the sponsorship of the National Institute of Mental Health. All misconceptions that the persistent movements of TD were rare, confusable with other drug-induced conditions such as parkinsonism, or inherently part of the patient's "schizophrenic condition" had been thoroughly disabused. All that remained was for the Food and Drug Administration and the drug industry to assume their responsibility to warn of the danger of tardive dyskinesia and prevent further needless crippling and disfigurement of thousands of American citizens, particularly elderly citizens. Neither did so with any expedition. Nearly four years passed before there were any changes in the Physician's Desk Reference to reflect that irreversible neurological effects could occur with phenothiazines, and almost five years went by before FDA formally issued any warning of the risk of TD and

93 George E. Crane, "Tardive Dyskinesia in Patients Treated with Major Neuroleptics: A Review of the Literature," American Journal of Psychiatry, v. 124, no. 8, Feb, 1968 suppl. George E. Crane, Minutes of the First Workshop on Tardive Dyskinesia, January 10-11, 1967, p. 58-59.

95 Ibid., p. 70.

"Neuroleptics-Antipsychotic drugs like Thorazine, Stellazine, Mellaril, Prolixin, etc. 97 George E. Crane and Russell Gardner, op. cit., p. 3.

" Ibid., p. 178.