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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 %
Children
(0-13)
Adolescents
(14-20)
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.

SSRIs and Persistent Pulmonary Hypertension of the Newborn (PPHN)

There’s a new study in the January 2014 issue of the BMJ:  Grigoriadis et al, Prenatal exposure to antidepressants and persistent pulmonary hypertension of the newborn: systematic review and meta-analysisThanks to Nanu Grewal for the link.

PPHN is a relatively rare condition.  The authors report that the estimated prevalence is about 1.9 per 1000 live births.  The disease is essentially a failure of the newborn’s circulatory system to switch from oxygen supply via the placental blood, to oxygen supply via the baby’s own lungs.  The condition is usually diagnosed at birth or shortly thereafter.  Symptoms include:  rapid and difficult breathing, fast heart rate, and blue skin color.  PPHN is a serious condition.  A 2010 article by Robin Steinhorn, MD, states:

“Even with appropriate therapy, the mortality for PPHN remains between 5-10%.  In addition, approximately 25% of infants with moderate or severe PPHN will exhibit significant neurodevelopmental impairment at 12-24 months.”

Delaney et al (2012) describe PPHN as “…a syndrome without either optimally effective preventative or treatment strategies,” and states that it “…remains a major cause of morbidity and mortality in neonatal centers across the globe.”

The BMJ article is a meta-analysis, combining the data from seven previous studies that examined the link between maternal use of SSRI’s and PPHN.  Here are their results:

 

SSRI Use Odds Ratio Confidence Interval 95% Statistical Significance
Early pregnancy 1.23 0.58-2.60 NS
Any time in pregnancy 1.55 0.79-3.04 NS
Most or all of pregnancy 3.33 1.58-7.02 S (0.002)
Late pregnancy 2.50 1.32-4.73 S (0.005)

 

Essentially what this means is that a woman who used SSRI’s for “most or all” of her pregnancy had a 3.33 times greater risk of delivering a child with PPHN than a woman who had not used SSRI’s.  The risk for late pregnancy use was 2.50 times greater.

Given a baseline prevalence estimate of 1.9 per 1000 births, and an odds ratio of 2.5, the expected incidence of PPHN in late-pregnancy SSRI cases would be about 4.75 (2.5 x 1.9).  This represents an excess of 2.85 cases per 1000 as compared to the general prevalence.

CONCLUSIONS

In the article’s abstract, the authors concluded:

“The risk of persistent pulmonary hypertension of the newborn seems to be increased for infants exposed to SSRIs in late pregnancy, independent of the potential moderator variables examined.  A significant relation for exposure to SSRIs in early pregnancy was not evident.”

In the text of the article a more detailed analysis was offered:

“Depression during pregnancy must not be left untreated, as the potential for untoward effects is not negligible and can extend into the postpartum period. Selection of treatment is based on several factors, and antidepressant drugs may be necessary, especially in severe depressive episodes…Although the odds for persistent pulmonary hypertension of the newborn seem to be greater with the use of SSRIs later in pregnancy, despite the limitations of the original studies, the risk is still low. Results from this meta-analysis still concur with earlier statements…that fewer than about 1 infant in 100 will develop persistent pulmonary hypertension of the newborn after antenatal exposure to SSRIs. Although this condition is serious and death rates between 5% and 10% have been reported, when it is associated with other conditions (such as some congenital malformations, meconium aspiration, sepsis, and idiopathic disease), it can be managed favourably…The death rate in infants with persistent pulmonary hypertension of the newborn who have been exposed to SSRIs, however, remains unknown (although one study did report 9.1% of the infants died who were exposed to SSRIs compared with 9.5% of those who were not exposed…”

The deference to the “need” for antidepressant drugs is noteworthy.  This kind of disclaimer has become almost routine in research of this kind.

In my view the essential point of the article is that it demonstrates one more serious adverse effect of these drugs.

Does Antidepressant Use Increase the Risk for Type 2 Diabetes?

On September 25, PsychCentral ran an article on this topic.  The article was a commentary on a 2013 meta-analysis conducted by Katharine Barnard, PhD, et al of the University of Southamptom, UK.

The meta-analysis examined three systemic reviews and 22 studies.

RESULTS

“There was evidence that antidepressant use is associated with type 2 diabetes. Causality is not established, but rather, the picture is confused, with some antidepressants linked to worsening glucose control, particularly with higher doses and longer duration, others linked with improved control, and yet more with mixed results. The more recent, larger studies, however, suggest a modest effect.”

CONCLUSIONS

“Although evidence exists that antidepressant use may be an independent risk factor for type 2 diabetes, long-term prospective studies of the effects of individual antidepressants rather than class effects are required. Heightened alertness to potential risks is necessary until these are complete.”

One more reason to be concerned about antidepressants!

SSRI’s During Pregnancy and APGAR Scores

There’s an interesting article on this topic by Hans Jensen et al, in the February 21, 2013 issue of the British Journal of Psychiatry.  You can see an abstract here.

The authors conducted a register study on all pregnant women in Denmark from 1996 to 2006, linking data from the Medical Birth Register, the Psychiatric Central Register, and the National Prescription Database.

They found that the

“… use of SSRIs during pregnancy increases the risk of a low Apgar score independently of maternal depression.”

APGAR scores were assessed five minutes after birth.

The APGAR score (named for Dr. Virginia Apgar) is a simple and reliable method to assess the health of a newborn baby.  It involves an assessment of appearance, pulse, grimace, activity, and respiration.

One more reason for not using SSRI’s.