Tag Archives: tardive dyskinesia

Neuroleptics and Tardive Dyskinesia in Children

There’s an interesting February 11, 2014, article on Peter Breggin’s website:  $1.5 Million Award in Child Tardive Dyskinesia MalpracticeThanks to Mad in America for the link.

Here’s the opening paragraph:

“On February 11, 2014 a Chicago jury awarded $1.5 million to an autistic child who developed a severe case of tardive dyskinesia and tardive akathisia while being treated by psychiatrists with Risperdal and then Zyprexa between 2002 and 2007. The drug-induced disorder was diagnosed when he was fifteen years old and by then had become disabling and irreversible.”

Tardive dyskinesia is a movement disorder characterized by repetitive, involuntary movements, including:  grimacing, tongue movements, chewing, lip smacking, puckering of the lips, purposeless limb and body movements, etc…  The movements are sometimes described as Parkinsonian-like.

Tardive akathisia involves feelings of inner restlessness that can range from a mild sense of inner discomfort to an almost unbearable feeling of generalized tension. Victims of this condition can seldom sit still.  They usually pace a great deal, sometimes for hours on end, and even when they sit or lie down, their limbs are in more or less constant motion.

Apparently the individual in Dr. Breggin’s paper was diagnosed with autism as a child and was prescribed SSRI’s before the age of seven.  The SSRI’s caused some deterioration in the child’s behavior and mental condition, to combat which his first psychiatrist prescribed Risperdal (risperidone).  Subsequently a second psychiatrist added Zyprexa (olanzapine) to the cocktail.  Both Risperdal and Zyprexa are neuroleptics (euphemistically known in psychiatric circles as antipsychotics), and are known to cause tardive dyskinesia.

On the face of it, one would think that this would be a big story.  One can picture the headline:  “Psychiatrists Destroy Child’s Brain.”  But in fact, the only references to this case that I’ve been able to find are the present article on Peter Breggin’s site, and links to Dr. Breggin’s article on Mad in America and Carl Elliott’s blog (Fear and Loathing in Bioethics).  Pharma’s stranglehold on the media is as effective as a government security blackout.

The truly tragic aspect of all this is that the neurotoxic effects of SSRI’s and neuroleptics are well known.  It’s not like the thalidomide tragedy of the early 1960’s, in which the teratogenic effects weren’t known until it was too late.  At which point, incidentally, the drug was taken off the market.

In the case of neuroleptics, or major tranquilizers as they used to be called, the link to tardive dyskinesia has been known for decades.  In fact, Jean Delay and Pierre Deniker, French psychiatrists who are generally “credited” with introducing neuroleptics into psychiatry in the early 1950’s, promoted the notion that the dyskinesic effect was linked to the putative therapeutic effect.  For this reason, they routinely raised the dose until this produced noticeable dyskinesia.

As the second generation neuroleptics became available, it was widely touted by pharma and by psychiatrists that these new drugs would not cause tardive dyskinesia.  That claim is now discredited.  The second generation neuroleptics do cause tardive dyskinesia, though perhaps at a slower rate than the earlier drugs. [CATIE Study]

The incidence of tardive dyskinesia among people who take neuroleptics is high.  The risk generally increases with higher doses and longer duration.  Psychiatrists justify this neurotoxification on the grounds of the “benefit” outweighing the risk, but it is truly difficult to imagine what benefit the individual in this case derived from these drugs that would outweigh his present plight.

Another argument that psychiatrists use in this area is that through careful observation, they can spot tardive dyskinesia in its very early stages, and by stopping the drug at that point, can arrest the problem.  The argument is specious, however, on two grounds.  Firstly, although the drugs cause this problem, they also mask its manifestation.  By the time the problem is sufficiently pronounced to break through the masking effect, it has already reached an advanced stage.  Secondly, the tardive dyskinesia is not only a disabling and disfiguring movement disorder, it is also an indication of more generalized neurological damage.  Here’s a quote from Joseph Glenmullen’s book Prozac Backlash (2000):

“We still do not fully understand how tics reflecting permanent brain damage develop with major tranquilizers.  But when one looks at the symptoms, the best model to explain them is that the appearance of noticeable tics is merely the final stage in a process of slow, progressive damage.” (p 57) [Emphasis added]

For readers who are not familiar with tardive dyskinesia, there are videos herehere, and here.  If you do a Google search, you can find others.

In my experience, there is a widespread belief among the general public that tardive dyskinesia is a “symptom” of the condition known as schizophrenia.  Almost everybody over the age of 40 who has been “diagnosed” as “schizophrenic” has been prescribed neuroleptics, and most of these people have tardive dyskinesia, so it’s not surprising that the public is confused.  Tardive dyskinesia is extraordinarily disfiguring and disabling, and serves to confirm the popular view – avidly promoted by psychiatrists – that “schizophrenia” is a progressive brain disease.  This is even more the case in that, as the victims of this neurotoxic assault continue to ingest these drugs, their presentation becomes steadily more disfiguring and more stigmatizing – “confirming” that “schizophrenia” is a progressive condition.

Organized psychiatry routinely claims that it is working hard to reduce the stigma associated with “mental illness,” and they castigate us “mental illness deniers” for allegedly increasing this stigma.  If psychiatry were seriously interested in destigmatizing these individuals, they would take some of the money that they are currently using to promote their profession, and use it to tell the public the truth:  that tardive dyskinesia is caused by psychoactive drugs!; that tardive dyskinesia is caused by psychiatrists and is entirely preventable.  But apparently the APA feel that they have better things to do with their money.

Psychiatry in America today is little more than a marketing arm for pharma.  Neuroleptics are neurotoxic drugs that, at least initially, have a controlling and dampening effect on agitated, aggressive behavior.  In the long term – and psychiatry routinely promotes them as long-term treatments – they are fraught with truly horrendous adverse potential.

Whatever might be argued about their use for consenting adults (and I recognize psychiatry’s creative understanding of the word “consent”), it’s difficult to even imagine how practitioners can foist these products onto children, whose brains are still developing.  By what kind of mental gymnastics can a psychiatrist prescribe these products to a child, and at the same time maintain even a semblance of self-esteem?

How much more destruction and how many more lawsuits is it going to take before psychiatrists recognize the obvious truth:  that you can’t help people by damaging their brains?  What is it about psychiatry that renders its adherents so narcissistically unreceptive to this patently clear reality?

In December 2012, Mark Olfson, MD, et al, published an article in the Archives of General Psychiatry.  The title is National Trends in the Office-Based Treatment of Children, Adolescents, and Adults with AntipsychoticsThe authors collected data from the National Ambulatory Medical Care Surveys for the period 1993-2009, and looked for trends in antipsychotic prescribing for children, adolescents, and adults in outpatient visits.  Here are the results:

Age Increase in no. of antipsychotic prescriptions per 100 population (1993-2009)
0-13 0.24-1.83 (almost 8-fold)
14-20 0.78-3.76 (almost 5-fold)
21+ 3.25-6.18 (almost 2-fold)


The authors provide a breakdown of the diagnoses assigned to the children and adolescents during the antipsychotic visits.

Diagnosis Visits %
Schrizophrenia 6.0 8.1
Bipolar 12.2 28.8
Depression 11.2 20.9
Anxiety 15.9 14.4
Dev Disorders 13.1 5.0
Disruptive Behavior Disorders 63.0 33.7
Other Dx’s 18.0 16.8


Percentages do not total 100, because some individuals were assigned more than one diagnosis.

As one can see, the most frequent use of these products for children of all ages, but especially for those under the age of 14, is disruptive behavior disorders.  In other words, the drugs are being used to control misbehavior.

On September 24, 2012, an article by Richard Friedman, MD, psychiatrist, appeared in the New York Times.  The article was titled A Call for Caution on Antipsychotic DrugsHere’s a quote:

“…there has been a vast expansion in the use of these second-generation antipsychotic drugs in patients of all ages, particularly young people. Until recently, these drugs were used to treat a few serious psychiatric disorders. But now, unbelievably, these powerful medications are prescribed for conditions as varied as very mild mood disorders, everyday anxiety, insomnia and even mild emotional discomfort.”

There is nothing to suggest that Dr. Friedman’s call for caution has been heeded.  In fact, according to Drugs.com, Abilify (aripiprazole), a second generation neuroleptic, was the best-selling drug in the US for all four quarters of 2013. (Q1, Q2, Q3, and Q4.)  Not just the best-selling psychiatric drug – the best selling drug, period!

Psychiatry is not something good that needs some minor corrections.  Psychiatry is something fundamentally flawed and rotten.  Organized psychiatry is so intoxicated by its own self-congratulatory rhetoric, that it has rendered itself blind to the reality – that it is destroying people’s brains.

Second Generation Neuroleptics, Tardive Dyskinesia, and the Law

There’s an interesting article on Harvard Law Petrie-Flom Center’s blog titled Daubert as a Problem for Psychiatrists.  It was written by Alex Stein and is dated September 19.  [Thanks to Dustin Salzedo for drawing my attention to this in a comment on an earlier post.]

The article deals with the legal rules governing the admission of expert testimony.  Apparently there are two different sets of rules in this area, known respectively as Frye and Daubert.

Under the Frye rules, expert testimony can be admitted only if its validity is generally recognized and accepted by the “relevant community of experts.”

Under the Daubert rules, testimony can be admitted if it is scientifically grounded and can be explained to a jury, even though it may still be controversial.

The importance of the distinction was highlighted in a recent United States District Court case – Patteson v Malloy.  In this case, Kay Patteson, plaintiff, had filed suit against her psychiatrist, John Maloney, MD, on the grounds that the Seroquel he prescribed her for insomnia had caused tardive dyskinesia.  Seroquel is a second-generation neuroleptic.  Tardive dyskinesia is an irreversible movement disorder involving disability and disfiguring involuntary movements.

When the second-generation neuroleptics first came on the market, it was claimed that they didn’t cause tardive dyskinesia, but the spuriousness of this claim was quickly recognized.  I certainly wasn’t aware that there was any residual controversy or doubt on this matter, but apparently there is – at least as far as Dr. Maloney is concerned.

In the court case, Dr. Maloney’s lawyers sought to have all testimony linking Seroquel to tardive dyskinesia excluded on the grounds that Ms. Patteson’s expert testimony was unreliable.  To support this position, Dr. Maloney produced his own expert whose study showed no link between Seroquel and Ms. Patteson’s tardive dyskinesia.  Dr. Maloney also contended that his expert’s study was sounder than the plaintiff’s.

Dr. Maloney, according to court documents, has contended that “…no scientific methodology has attributed Seroquel to causing tardive dyskinesia.”  He has also indicated that the study his expert witness will present is a “…– a clinical trial conducted by AstraZeneca…” (the manufacturer and marketer of Seroquel).  Dr. Maloney’s expert witness is Thor W. Rak, MD.

I can find no information on the Internet about Dr. Rak.  Nor have I been able to identify the particular AstraZeneca trial.

On September 16, 2013, the judge ruled that the scientific evidence linking Seroquel to tardive dyskinesia is solid enough to be presented to a jury.  The judge also allowed testimony on differential diagnosis to be admitted.  This involves systematically ruling out other possible causes of the tardive dyskinesia, leaving only Seroquel as the remaining causative agent.

It is unlikely that these rulings would have been made under the Frye rules.

Back to Alex Stein’s article.

“The consequent liability risk for psychiatrists is obvious, given the frequency of tardive dyskinesia among psychiatric patients. Antipsychotic drug prescriptions follow the trial and error method. This method involves patient-specific observations, tradeoffs and adjustments that rely on the psychiatrist’s intuition. There are no hard-and-fast rules and protocols similar to those that provide legal ‘safe harbors’ for other doctors…As a result, plaintiffs’ experts would often be able to second-guess the psychiatrist’s drug prescription and plausibly describe it as negligent.”

Dr. Stein goes on to point out that the increased liability risk for psychiatrists will now apply in state and federal courts that use the Daubert rules.  Dr. Stein points out that psychiatrists, before prescribing neuroleptics, can protect themselves from this liability by having their clients sign an informed consent document that explains the risk of tardive dyskinesia.


It is a general theme of this website that psychiatric drugs are not medications in any proper sense of the word.  Rather, they are neurotoxic chemicals with a wide range of negative effects.

One of these effects, that in my opinion is particularly devastating, is tardive dyskinesia. If you’re not familiar with this condition, you can see some video footage here.  If you do a Google search, you will find more videos.  It has been known for decades that neuroleptic drugs (i.e. the class of drugs used to “treat” the so-called psychotic disorders) cause tardive dyskinesia.  As mentioned earlier, this includes the second-generation neuroleptics.

I have always been troubled by the ease with which psychiatrists prescribe these products and the vehemence with which they defend these practices.  In recent decades, I have been frankly appalled by the fact that psychiatry has been systematically expanding the range of problems for which they prescribe these drugs, even to the point of administering them to toddlers to control temper tantrums, and elderly dementia patients to control agitation and aggression.

These expansions have attracted a good measure of criticism, which psychiatry routinely ignores, though in very recent months there have been some indications of retreat.  (See the APA’s news release List of Common Uses of Psychiatric Medications to Question.)

But of its own accord, psychiatry seldom takes note of the damage that it does.  With the easing of the rules on evidence admission, it may be that successful malpractice suits will prevail where considerations of “do no harm” have failed.

Tardive Dyskinesia

In the late 80’s, I worked for a while in a State Hospital in West Virginia.  Clients would arrive on 72-hour holding committals from the counties, and if the psychiatrist felt that the client needed to stay longer than that (which was almost always the case), then either the client had to convert to voluntary status, which is what happened in most cases, or the hospital had to arrange for a hearing in front of a judge.  For convenience, a local judge would come in and the hearing would be held in the hospital.

At the hearing there would be an attorney representing the hospital’s position, and another attorney appointed by the court to represent the client.  In theory it was a fair procedure, but in general, defense lawyers tended to be overawed by psychiatric testimony, and it was my impression that the hospital’s petition for committal was usually granted.

I got to know some of the attorneys slightly, and one day as I was walking out of the hospital to get lunch, I encountered one of them (let’s call him Steve) who was also going to lunch.  We went to a sandwich shop and chatted while we ate.

In the course of conversation Steve expressed a measure of admiration for mental health workers because “it’s all so hopeless.”

“Why do you say that?” I asked.

“Well their brains are damaged.  They’re not going to get better,” Steve replied.

“Why do you say their brains are damaged?”

“Well you can see it,” he said.  “The way they grimace and make those awful chewing movements!”

So I spent the next ten minutes or so telling Steve about tardive dyskinesia – an irreversible neurological disorder which causes disfiguring and stigmatizing rhythmic, involuntary movements of the neck, hands, limbs, torso, and face (including grimaces and chewing).  And I told him that this condition is caused by the major tranquilizers that are administered to many hospital clients, often involuntarily.

His reaction was one of shocked disbelief.

You mean it’s the treatment that makes them like that?”

I nodded.

Since then I have encountered a good many individuals who were not aware that this condition was caused by the so-called anti-psychotic drugs.

So – just in case there are any people who don’t know about tardive dyskinesia, here’s a brief synopsis.

Tardive dyskinesia is a movement disorder which arises from damage to brain cells in the extrapyramidal system (i.e. the neurons that control fine motor adjustment).  The presentation varies from person to person, but generally involves involuntary rhythmic motions of fingers, hands, lips, tongue, head, and neck.  In some cases squirming movements of the legs and torso are also evident.  The condition is irreversible.

Tardive dyskinesia is caused by the ingestion of major tranquilizers (also known as neuroleptics and anti-psychotics).  In general, the higher the dose and the longer the “treatment,” the greater the risk of developing tardive dyskinesia, but the condition has been known to develop after relatively low doses for short durations.

Although the drug causes the damage, it also, to some extent, masks the condition.  So sometimes the onset is not apparent until the drug is stopped.

If you have never seen a person with tardive dyskinesia, there is a video on the Internet here.  If you Google around you’ll find more videos.

It is extremely disfiguring and stigmatizing.