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). 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
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(1992) Task force on tardive dyskinesia. Washington
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Breggin, P. R. (1983) Psychiatric
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560
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Press |
Peter R. Breggin, MD 101 East State Street,
PMB 112 Ithaca, New York 14850 By Appointment Only Phone
607 272 5328 Fax 607 272
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