[SSRI-Research] The Dangers of Anti-Psychotic Drugs - by Peter Breggin, MD

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[sSRI-Research] The Dangers of Anti-Psychotic Drugs - by

Peter Breggin, MD

 

 

 

 

 

Preventive Psychiatry E-Newsletter # 170

 

Should the Use of Neuroleptic Drugs Be Severely Limited?

 

by Peter R. Breggin, M.D.

 

Ed. Note: Psychotropic drugs should never be abruptly discontinued or

tapered off without the help of a knowledgeable physician, preferably

the prescribing physician, who understands what these drugs do at the

molecular and synapse level. - GGK

 

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.

 

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.

 

____________________________

 

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.

 

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

 

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B. (1975) Mental illness in the biological and adoptive families of

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New York Times A, 22

 

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