Neuroleptics

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WARNING!

When trying to withdraw from many psychiatric drugs, patients can develop

serious and even life-threatening emotional and physical reactions. In short, it

is dangerous not only to start taking psychiatric drugs but also can be

hazardous to stop taking them. Therefore, withdrawal from psychiatric drugs

should be done under clinical supervision. Principles of drug withdrawal are

discussed in Your Drug May Be Your Problem: How and Why to Stop Taking

Psychiatric Medications, by Peter R. Breggin, M.D. and David Cohen, Ph.D. Other

information on Prozac and Prozac-like drugs can be found in Talking Back to

Prozac by Peter R. Breggin, M.D. and Ginger Ross Breggin.

 

Should the use of neuroleptics be severely limited?

by Peter R. Breggin, M.D.

This article was first published in Controversial Issues in Mental Health edited

by Stuart A. Kirk and Susan D. Einbinder (pub. Allyn and Bacon) and is reprinted

with kind permission. It is an updated version of a talk given for the

Shropshire Mental Health Institute.

 

 

 

 

 

 

 

 

 

The neuroleptic drugs have gradually become promoted as agents with a specific

" antipsychotic " effect on schizophrenic symptoms. Meanwhile, psychosocial

approaches have fallen into disrepute among many psychiatrists. Patients have

been instructed to remain on neuroleptics for a lifetime and told that it was

safe to do so. The public was told that the " miracle " drugs had emptied the

hospitals and returned millions of patients to normal lives.

the reality

In 1973, psychiatrist George Crane gained the attention of the medical community

by disclosing that many, and perhaps most, long-term neuroleptic patients were

developing a largely irreversible, untreatable neurological disorder, tardive

dyskinesia (Crane, 1973). The disease, even its mild forms, is often

disfiguring, with involuntary movements of the face, mouth or tongue.

Frequently, the patients grimace in a manner that makes them look " crazy " ,

undermining their credibility with other people. In more severe cases, patients

become disabled by twitches, spasms, and other abnormal movements of any muscle

groups, including those of the neck, shoulders, back, arms and legs, and hands

and feet (American Psychiatric Association, 1992; Breggin, 1983; 1990; 1991).

The muscles of respiration and speech can also be impaired. In the worst cases,

patients thrash about continually.

The rates for tardive dyskinesia are astronomical. The latest estimate from the

American Psychiatric Association (1992, p. 68) indicates a rate for all patients

of five per cent per year, so that 15 per cent of patients develop tardive

dyskinesia within only three years. In long-term studies, the prevalence of

tardive dyskinesia often exceeds 50 per cent of all treated patients and is

probably much higher. The disease affects people of all ages, including

children, but among older patients rates escalate. In a controlled study, 41 per

cent of patients aged 65 and older developed tardive dyskinesia in a mere 24

months (Yassa et al., 1988). Hundreds of thousands of older people receive these

drugs in nursing homes and state hospitals.

Other closely related, untreatable neurological disorders have now been

recognized as variants of tardive dyskinesia. Tardive akathisia involves painful

feelings of inner tension and anxiety and a compulsive drive to move the body.

In the extreme, the individual undergoes internal torture and can no longer sit

still. Tardive akathisia often develops in children who have been treated for

" hyperactivity " , ironically and tragically subjecting them to permanent inner

torture. Tardive dystonia involves muscle spasms, frequently of the face, neck

and shoulders, and it too can be disfiguring, disabling and agonizing.

There are no accurate surveys of the total number of patients afflicted with

tardive dyskinesia. There are probably a million or more tardive dyskinesia

patients in the United States today, and tens of millions have been afflicted

throughout the world since the inception of neuroleptic treatment (Breggin,

1991). Despite this tragic situation, psychiatrists too often fail to give

proper warning to patients and their families. Often psychiatrists fail to

notice that their patients are suffering from tardive dyskinesia, even when the

symptoms are flagrant (Brown and Funk, 1986; Breggin, 1991).

In 1983 I published the first in-depth analysis of the vulnerability of children

to a particularly virulent form of the tardive dyskinesia that attacks the

muscles of the trunk, making it difficult for them to stand or walk. This is now

an established fact. In the same medical book, I offered the first detailed

documentation showing that many or most tardive dyskinesia patients also show

signs of dementia—an irreversible loss of overall higher brain and mental

function. Indeed, it was inevitable that these losses would occur. The basal

ganglia, which are afflicted in tardive dyskinesia, are richly interconnected

with the higher centres of the brain, so that their dysfunction almost

inevitably leads to disturbances in cognitive processes (for the functional

neuroanatomy, see Alheid et al., 1990). Since my observations, a multitude of

studies have confirmed that long-term neuroleptic use is associated with both

cognitive deterioration and atrophy of the brain (Breggin, 1990; Gualtieri and

Barnhill, 1988). While defenders of the drugs sometimes claim that this mental

and neurological deterioration is caused by schizophrenia itself, their position

is untenable. More than 100 years of autopsy studies of patients labelled as

schizophrenic failed to show any such deterioration, until the recent advent of

neuroleptics.

Growing evidence indicates that these drugs produce tardive psychoses that are

irreversible and more severe than the patients' prior problems. In children,

permanent behavioral or mental disorders frequently develop as a result of the

drugs (Gualtieri and Barnhill, 1988). Furthermore, drug withdrawal often causes

rebound of the anticholinergic neurotransmitter system, resulting in a flu-like

syndrome that includes emotional upset, insomnia, nausea and vomiting. Many

patients find themselves unable to stop taking the drugs, suggesting that we

should consider them as addictive (Breggin, 1989a, 1989b).

Shocking as it may seem, this brief review can only scratch the surface of

neurological disorders associated with these drugs, let alone the vast number of

other potentially serious side effects. For example, in a small percentage of

patients the neuroleptic reaction goes out of control, producing neuroleptic

malignant syndrome. The disorder is indistinguishable from an acute inflammation

of the brain comparable to lethargic encephalitis (Breggin, 1990, 1991) and can

be fatal. Given that these are exceedingly dangerous drugs, what about their

advantages? How do they " work " ? It is well known that these drugs suppress

dopamine neurotransmission in the brain, directly impairing the function of the

basal ganglia and the emotion-regulating limbic system and frontal lobes and

indirectly impairing the reticular activating system as well. The overall impact

is a chemical lobotomy—literally so, since frontal lobe function is suppressed

(Breggin, 1983, 1991). The patient becomes de-energized or de-enervated. Will or

volition is crushed, and passivity and docility are induced. The patient

complains less and becomes more manageable. Despite the claims made for symptom

cure, multiple clinical studies document a non-specific emotional flattening or

blunting effect (reviewed in Breggin 1983, 1991).

There is no significant body of research to prove that neuroleptics have any

specific effect on psychotic symptoms, such as hallucinations and delusions. To

the contrary, these remain rather resistant to the drugs. The neuroleptics

mainly suppress aggression, rebelliousness, and spontaneous activity in general.

This is why they are effective whenever and wherever social control is at a

premium, such as in mental hospitals, nursing homes, prisons, institutions for

persons with developmental disabilities, children's facilities and public

clinics, as well as in Russian and Cuban psychiatric political prisons. Their

widespread use for social control in such a wide variety of people and

institutions makes the claim that they are specific for schizophrenia

ridiculous. (They are even used in veterinary medicine to bend or subdue the

will of animals. When one of our dogs was given a neuroleptic for car sickness,

our daughter observed, " He's behaving himself for the first time in his life " .)

The neuroleptics are supposedly most effective in treating the acute phase of

schizophrenia, but a recent definitive review of controlled studies showed that

they perform no better than sedatives or narcotics and even no better than

placebo (Keck et al., 1989). One psychiatrist (Turns, 1990) responded to these

revelations with anguished questions: " Has our clinical judgement about the

efficacy of antipsychotics been a fixed, encapsulated, delusional perception . .

.. Are we back to square one in antipsychotic psychopharmacology? " .

That the neuroleptics emptied the U.S. mental hospitals is a myth. The drugs

were in widespread use as early as 1954 and 1955, but the hospital population

did not decline until nearly ten years later, starting in 1963. That year the

federal government first provided disability insurance coverage for mental

disorders. The States could at last relieve themselves of the financial burden

by refusing admission to new patients and by discharging old ones. The

discharged patients, callously abandoned by psychiatry, received a small federal

cheque for their support in other facilities, such as nursing or board and care

homes. Some patients went home as dependents while others went onto the streets.

Follow-up studies show that very, very few patients became independent or led

better lives following these new policies (Mosher and Burti, 1989, Breggin,

1991).

But are there better psychosocial alternatives? Controlled studies by Loren

Mosher have shown that patients diagnosed with acute schizophrenia improve

better without medication in small home-like settings run by non-professional

staff who know how to listen and to care (Mosher and Burti, 1989). The patients

become more independent, and do so at no greater financial cost, because

non-professional salaries are so much lower. As an enormous added benefit, the

drug-free patients do not get tardive dyskinesia or tardive dementia, as well as

other drug-induced and sometimes life-threatening disorders.

Controlled studies by Karon and Vandenbos (1981) indicate that even in

traditional psychiatric facilities psychotherapy is the treatment of choice for

patients labelled as schizophrenic. My own experience in psychiatry began as a

college student volunteer in a State mental hospital. We proved that untrained

college students, with only minimal supervision, could work as case aides to

help nearly all of our chronic patients leave the hospital (Breggin, 1991).

But isn't schizophrenia a biochemical and genetic disease? In reality, there's

no convincing evidence that schizophrenia is a biochemical disorder. While there

are a host of conjectures about biochemical imbalances, the only ones we know of

in the brains of mental patients are those produced by the drugs. Similarly, no

substantial evidence exists for a genetic basis of schizophrenia. The frequently

cited Scandinavian genetic studies (Kety et al., 1975; reviewed in Breggin,

1991) actually confirm an environmental factor while disproving a genetic one.

Such conclusions may seem incredible to readers who have been bombarded with

psychiatric propaganda, and I can only hope they will personally review the

literature and read Toxic Psychiatry for a review and analysis. But even if

schizophrenia were a brain disease, it would not make sense to add further brain

damage and dysfunction by administering neuroleptics.

If the neuroleptics are so dangerous and have such limited usefulness, and if

psychosocial approaches are relatively effective, why is the profession so

devoted to the drugs? The answer lies in maintaining psychiatric power,

prestige, and income. What mainly distinguishes psychiatrists from other mental

health professionals, and of course from non-professionals, is their ability to

prescribe drugs. To compete against other mental health professionals,

psychiatry has wed itself to the medical model, including biological and genetic

explanations, and physical treatments. It has no choice: anything else would be

professional suicide. In providing psychosocial therapies, psychiatry cannot

compete with less expensive, more helpful non-medical therapists, so it must

create myths that support the need for medically trained psychiatrists.

After falling behind economically in competition with psychosocial approaches,

psychiatry formed what the American Psychiatric Association now admits is a

" partnership " with the drug companies (Sabshin, 1992). Organized psychiatry has

become wholly dependent for financial support on this unholy collaboration with

the pharmaceutical industry (Breggin, 1991). To deny the effectiveness of drugs

or to admit their dangerousness would result in huge economic losses on every

level from the individual psychiatrist who makes his or her living by

prescribing medication, to the American Psychiatric Association which thrives on

drug company largesse.

If neuroleptics were used to treat anyone other than mental patients, they would

have been banned a long time ago. If their use wasn't supported by powerful

interest groups, such as the pharmaceutical industry and organized psychiatry,

they would be rarely used at all. Meanwhile, the neuroleptics have produced the

worst epidemic of neurological disease in history. At the least, their use

should be severely curtailed.

Beyond the specific issue of the neuroleptics, there is a much broader one— how

are we to understand and to show care for people who undergo emotional pain and

anguish (Breggin, 1991,1992; Mosher and Burti, 1989). Are we to view them as

defective objects or as human beings struggling with emotional and social

problems and personal conflict? Are we to drug them into oblivion, or are we to

understand and empower them? Giving a drug disempowers the recipient. It says,

" You are helpless in the face of your problems. You need less feeling and

energy, and less brain function " . The true aim of therapy should be to

strengthen and to empower the individual. People, not pills, are the only source

of real help.

references

Alheid, G. F., Heimer, L. and Switzer, 111, R. D. Basal ganglia. In G. Paxinos

(ed.) The human nervous system. New York: Academic press

American Psychiatric Association (1992) Task force on tardive dyskinesia.

Washington DC: APA

Breggin, P. R. (1983) Psychiatric drugs. New York: Springer

Breggin, P. R. (1989a) Addiction to neuroleptics? (letter) American Journal of

Psychiatry, 146, 560

Breggin, P. R. (1989b) Dr Breggin replies (follow-up letter on addiction to

neuroleptics). American Journal of Psychiatry, 146,1240

Breggin, P. R. (1990) Brain damage, dementia and persistent cognitive

dysfunction associated with neuroleptic drugs. Evidence, etiology, implications.

Journal of Mind and Behavior, 11, 425 64

Breggin, P. R. (1991) Toxic psychiatry. New York: St Martin's Press

Breggin, P. R. (1992) Beyond conflict. New York: St Martin's Press

Brown, P. and Funk, S. C. (1986) Tardive dyskinesia: barriers to professional

iatrogenic disease. Journal of Health and Social Behavior, 27,11032

Crane, G. (1973) Clinical psychopharmacology in its 20th year. Science, 181,121

8

Gualtieri, C. T. and Barnhill, L. J. (1988) Tardive dyskinesia in special

populations. In M. E. Wolf and A. D. Mosnaim (eds) Tardive dyskinesia.

Washington DC: American Psychiatric Press

Karon, B. and Vandenbos, G. (1981) The psychotherapy of schizophrenia. New York:

Jason Aronson

Keck, P. E. Jr., Cohen, B. M. and Baldessarini, R. (1989) Tirne course of

antipsychotic effects of neuroleptic drugs. American Journal of Psychiatry,

146,1289-92

Kety, S., Rosenthal, D., Wender, P., Schulsinger, F. and Jacobsen, N. B. (1975)

Mental illness in the biological and adoptive families of adopted individuals

who have become schizophrenic. In E. Fieve, D. Rosenthal and H. Brill (eds)

Genetic research in psychiatry. Baltimore: Johns Hopkins

Mosher, L. R. and Burti, L. (1989) Community mental health. New York: Norton

Sabshin, M. (1992, 10 March) To aid understanding of mental disorders. New York

Times A, 22

Turns, C. N. (1990) Effects of sedatives and neuroleptics (letter). American

Journal of Psychiatry, 147, 1576

Yassa, R., Nastase, C., Camille, Y. and Belzile, L. (1988) Tardive dyskinesia in

a psychogeriatric population. In M. D. Wolf and A. D. Mosnaim (eds) Tardive

dyskinesia. Washington DC: American Psychiatric Press

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