Tag Archives: akathisia

My Response to a Defender of Psychiatry

On October 13, an interesting article was published on the Huffington Post Blog.  The author is Jessica Gold, MD, a psychiatry resident at Stanford University; the post is titled Inpatient Psychiatry: Not all Needles, Drugs And Locks.

The article is a personal experience/opinion piece, the gist of which is that people who criticize or condemn psychiatry simply don’t understand the complexities and needs of psychiatry’s “patients”, particularly the need for locked wards.

The article is generally unremarkable in that the arguments adduced are well-worn by more senior psychiatrists.  But it is interesting, and indeed tragic, to see a new entrant to the field absorbing psychiatry’s defensive nonsense, and trotting it out uncritically for public consumption.

. . . . . . . . . . . . . . . .

Dr. Gold begins by describing the kinds of interactions she experiences in social settings when people learn that she is a psychiatrist.


“However, what frustrates me most are the times when after describing my day-to-day as a psychiatry resident, I am met with bewilderment, followed by misplaced sarcasm as I am asked, ‘And why would you want to do that?'”

Dr. Gold then becomes reflective:

“After reminding myself not to get defensive (as I continued to do throughout writing this piece) or just stop the conversation completely, I became intrigued. While doctors may not evoke the same respect and adoration of the days of house visits, no one asks the other doctors (non-psychiatrists) in my family with such strong negative connotation why they chose their respective specialties.

I began to wonder if it’s because the difference between a locked ward and a medical ward can seem confusing and scary to an outsider or a patient. Without knowing the safety rationale, it can feel degrading to have your clothes taken away, along with your cell phone, shoelaces, and sharp objects, only to sleep in a boring room with heavy, non-moveable (or throw-able) furniture. If you lack insight into your illness and do not understand the necessity of hospitalization, it can feel prison-like to be on a locked ward without the ability to leave it. And, without understanding the therapeutic benefit of engaging in connections with others on the unit, it can feel restrictive to have visiting hours and not be able to have a significant other or family member spend the night.”

So Dr. Gold is frustrated by the sarcasm she encounters when social acquaintances discover that she is a psychiatrist, and notes that other medical specialties do not generally attract this kind of response. She wonders if the reason for this differential response might be:

“… because the difference between a locked ward and a medical ward can seem confusing and scary to an outsider or a patient.”

This is a truly delightful piece of self-deceptive spin.  Psychiatry’s so-called patients might well feel scared of locked wards, and understandably so.  But the notion that fears of this sort underlie the general public’s negative perception of psychiatry is arrant nonsense.  The general public’s negative perception of psychiatry, as compared to genuine medical specialties, is grounded in a realistic appraisal of psychiatry’s spurious concepts and destructive “treatments”.  In particular, psychiatry is negatively perceived because:

  1. Psychiatry’s definition of a mental disorder/ illness, as set out in DSM III, IV, and 5, embraces virtually every significant problem of thinking, feeling, and/or behaving. Psychiatry uses this definition to fraudulently medicalize problems that are not medical in nature.
  1. Psychiatry routinely presents these so-called illnesses as the causes of the specific problems, when in fact they are merely labels: abbreviated rewordings of the presenting problems with no explanatory function or value.  These labels, which cause enormous damage to the individuals to whom they are assigned, serve only to legitimize the pushing of drugs, and to enable psychiatrists to bill for the services they provide.  Unlike real diagnoses, they provide no insight into the nature or essence of the presenting problems, but are nevertheless defended tenaciously by psychiatrists and their pharma funders.
  1. Psychiatry has routinely deceived, and continues to deceive, their clients, the public, the media, and government agencies, that these vaguely defined problems are in fact illnesses with known neural pathology. The classic example of this is the chemical imbalance theory of depression – a blatant hoax which was pushed so heavily by psychiatry that it has now become “common knowledge”.  And the most noteworthy aspect of this is that although the hoax has been exposed repeatedly – (most recently by Terry Lynch in his book Depression Delusion), psychiatry has taken no concerted steps to correct this misinformation, and indeed in many quarters is still promoting this fiction as established medical fact.
  1. Psychiatry has blatantly promoted drugs as corrective measures for these illnesses, when in fact it is well-known in pharmacological and psychiatric circles that no psychiatric drug corrects any neural pathology. In fact, the opposite is the case.  All psychiatric drugs exert their effect by distorting or suppressing normal brain functioning.  It is also well known that the adverse effects of these products are often devastating and permanent.
  1. Psychiatry has collaborated and conspired with pharma in the development of a vast body of fraudulent research, all designed to “demonstrate” that psycho-pharmaceutical products are safe and effective. The methods by which this fraud has been perpetrated include:  the routine suppression of negative results; the use of ridiculously short follow-up intervals; over-stating of marginal results; suppression of adverse effects; etc., etc.
  1. A great many psychiatrists have shamelessly accepted large sums of pharma money for very questionable activities. These activities include the widespread presentation of pharma infomercials in the guise of CEUs; the ghost-writing of books and papers which were actually written by pharma employees; targeting of captive and vulnerable audiences in nursing homes, group homes, and foster-care systems for prescription of psychiatric drugs; etc., etc…   Two glaring examples of this kind of venality are:

In this context, it should be noted that Dr. Biederman and Dr. Frances are among the most eminent and prestigious psychiatrists in the US.

In addition, 70% of the DSM-5 task force members had received funding from the pharmaceutical industry.

  1. Psychiatry’s labels are inherently disempowering. To tell a person, who in fact has no biological pathology, that he has an incurable illness, for which he must take psychiatric drugs for life, is an intrinsically disempowering act which robs people of hope, and encourages them to settle for a life of drug-induced dependency and mediocrity.
  1. Psychiatry’s “treatments”, whatever transient feelings of well-being or tranquilization they may induce, are always destructive and damaging in the long-term. Neuroleptic drugs cause tardive dyskinesia.  Extended use of antidepressants produces a state of chronic joylessness.  Benzodiazepines are addictive.  High-voltage electric shocks to the brain erase memories.  Psychiatry’s notion that one can solve people’s problems by tinkering irresponsibly with their brains, betrays a degree of arrogant naivety unequalled in other professional groups.
  1. Psychiatry’s spurious and self-serving medicalization of every significant problem of thinking, feeling, and/or behaving, effectively undermines human resilience, and fosters a culture of powerlessness, uncertainty, and dependence. Powerful, time-honored concepts such as the need for critical self-appraisal, and personal improvement through effort, have been systematically marginalized by psychiatry’s expanding list of “illnesses”, and ever-flowing supply of drugs.  Relabeling as illnesses, problems which previous generations accepted as matters to be addressed and worked on, and harnessing billions of pharma dollars to promote this false message, is morally and professionally repugnant.
  1. Psychiatry’s primary agenda over the past four or five decades has been the expansion of its list of “illnesses”, and the assignment of these illnesses to more and more people. It has now become routine practice to prescribe neuroleptic drugs to elderly nursing home residents who become “unmanageable”, and to young children for temper tantrums!

This is the profession that Dr. Gold chose to enter and now chooses to defend with patronizing platitudes.

. . . . . . . . . . . . . . . .

Back to Dr. Gold’s paper:

“Dear future and past patients: I. COMPLETELY. GET. IT. Nothing about being on a psychiatric ward is typical, even for a medical setting. But I (and every nurse, social worker, psychologist, occupational therapist, physical therapist, nursing assistant, and physician I have ever worked with) also really want to help you. That is why I chose a career in medicine, and even more true of the reason why I chose to specialize in psychiatry. I worry the images you have of inpatient psychiatry scare you and prevent you from seeing me as an ally. Even when I tell you that I am here to help, I can see the skepticism in your eyes and hear the fear in your voice. I am trained to observe, after all.

It is not surprising, then, that when I read descriptions or see my job portrayed as forceful or horrific, I want to take the time to correct them. I am not doing this simply because I want to protect my profession, but am actually doing this in defense of and in support of anyone who might need mental health help in the future. Stigmatizing attitudes toward psychiatric illnesses already exist; fear of psychiatry and seeking care do not need to be added to the equation.”

In recent years, the psychiatric survivor movement has grown, both in numbers and in the volume of output.  Survivors are writing about the mistreatment they have received, often for decades, at the hands of psychiatry.  But Dr. Gold dismisses these protests as erroneous and misinformed over-reactions.  Psychiatry’s so-called patients:  “lack insight” into their illnesses; do not understand “the necessity of hospitalization”; do not understand “the therapeutic benefit of engaging in conversations with others on the unit”; don’t realize that the psychiatrists who authorized the forcible injection of akathisia-inducing drugs “really” want to help; etc..

And Dr. Gold is taking the time to correct these misperceptions, not simply because she wants to protect her profession (Heavens, no!), but rather in defense and support of anyone who might need psychiatric help in the future.  How noble!

“Maybe people will always fear psychiatry, mental illness and what they do not know…But maybe those attitudes can be changed and as mental health advocates, we need to do everything we can to assuage those fears. Unfortunately, even well-meaning former patients perpetuate those fears, whether inadvertently or because of the limited lens through which they viewed their own hospitalization.”

To which I might respond:  Even well-meaning psychiatrists perpetuate these fears, whether inadvertently or because of the erroneous and destructive disease-focused lens through which they view their “patients” and their “treatments”.

The rationalizations and self-justifications continue:

“I’ve been screamed at, cursed at, rushed towards, demeaned and have seen patients and nurses get seriously injured.  Even still, I do not make these decisions lightly or lead a conversation with a needle.”

The great irony here is that the neuroleptic drugs that psychiatrists routinely use to control aggressive behavior frequently produce a condition called akathisia, which in turn is a known precipitator of suicide and violence.  Crowner, Douyon, et al, conducted a short study of this matter in 1990.  Here’s a quote from their paper:

“Akathisia is a common side effect of neuroleptic drugs that may present with behavioral disturbances. There have been preliminary reports on the association between violence and akathisia. We report the first observational study of this relationship. Patients studied were from a special unit for violent patients. A closed-circuit television camera was installed in each of the corners in its dayroom. Incidents of assault plus the 5 minutes preceding each assault were recorded on videotape. Participants and bystanders were rated for the motor component of akathisia. For each of nine incidents, we compared the akathisia scores for participants and for bystanders. Both victims and assailants were akathisic before about half of all incidents; bystanders rarely were. The classification of the movements we rated and the implications for further studies are discussed.”

It would be interesting to know how many of the individuals who screamed, cursed at, rushed towards, and demeaned Dr. Gold were experiencing akathisia as a result of neuroleptic or antidepressant drugs that she had prescribed for them.  It is also interesting that no major follow-up of the Crowner, Douyon, et al study has been undertaken by psychiatry.

. . . . . . . . . . . . . . . .

“Given the responses to our career selection in casual conversation, it is probably not shocking that I (and my peers) can sometimes hesitate to say my medical specialty, despite having no shame or regrets about my decision. Knowing now that hiding my profession only further contributes to its stigma, and without a voice or a face, psychiatrists and their patients will always just be a part of a power struggle…, I will never again shy away from it:

I am a psychiatrist-in-training. My job is complicated, weird, unique, fun, fulfilling, and challenging… but that’s what makes it beautiful.”

Well all of this is nice to know, but in my view, psychiatry is neither fun nor fulfilling for those on the receiving end, especially in the long-term..

. . . . . . . . . . . . . . . .

The reality is that psychiatry is not something good that needs some minor corrections.  Rather, it is something fundamentally flawed and rotten; a wrong turning in human history, trailing death, disability, and disempowerment in its worldwide wake.  No amount of rationalization or platitudinous exculpations can mitigate this reality.  Psychiatry kills people every day, and adamantly refuses to recognize this reality and take appropriate action.


Neuroleptic Drugs, Akathisia, and Suicide and Violence

Thirty-three years ago, in August 1983, an article titled Suicide Associated with Akathisia and Depot Fluphenazine Treatment appeared in the Journal of Clinical Psychopharmacology.  The authors were Katherine Shear, MD, Allen Frances, MD, and Peter Weiden, MD.

Here are some quotes, interspersed with my comments/observations:

“Akathisia is a common and distressing side effect of neuroleptic medication that can be difficult to recognize and treat.  Several previous reports mention maladaptive behavioral consequences, such as poor compliance with prescribed medication and aggressive or self-destructive outbursts.  We are reporting suicides in two young Hispanic men who had developed severe akathisia after treatment with depot fluphenazine.  Depression with suicidal behavior has been observed following fluphenazine injection, but suicide associated with akathisia has not been previously noted.”

Fluphenazine is a neuroleptic drug of the phenothiazine class that was introduced in 1959.  It is marketed as Prolixin and other brand names, and according to Wikipedia, is on the WHO’s “List of Essential Medicines, most important medications needed in a basic health system.”

The “treatment” used in each case was a depot injection of fluphenazine.  This is a long-lasting injection, typically 30 days, in which the drug is lodged in a dermal or muscular mass from which it is slowly drawn into the blood stream.  (Hence depot:  a place where goods are stored for later distribution.)

Depot injections have some obvious convenience value, but in psychiatry are usually used to ensure compliance.  Their major downside is that if the person has an adverse reaction to the drug, there’s no way to remove the stored chemicals from his body.

The authors may be correct in stating that this is the first published report of suicide associated with akathisia, but it is not the first report of suicide associated with fluphenazine.  Seventeen years earlier, Dorothy West, MD, had published the following letter in the British Journal of Psychiatry, 117 (1970), 718-9.


Dear Sir,

A new drug is being widely used in the treatment of mental illness.  It is long-acting and used by injection – its name is fluphenazine (Moditen).  Is this the thalidomide of the 70’s?  I would like to have the opinion of other doctors.  Whilst it is still new maybe we are lulled into a false sense of security, but are we justified in using a drug, which may take up to six weeks to eradicate from the tissues, without being sure of its safety?  Its side effects alone are legion.  A study of 13 papers gives the following:
Common side-effects reported are – lethargy, drowsiness, dizziness, muscular inco-ordination, paraesthesia, hypotension, blurring of vision, dryness of mouth, malaise, feelings of tension, confusion, nausea, vomiting, and aches and pains.
Parkinsonism is extremely common.  Incidence in reports varies from 100 per cent to 24 per cent with many reports around 50 per cent.
Depression is quite common and tends to be severe – 5 suicides reported and two suicide attempts.
Other reported side-effects include psychotic relapse and glaucoma.

Dorothy West”

. . . . . . . . . . . . . . . .

Back to the Shear, Frances, and Weiden paper:

Case Reports

“Case 1

A 23-year-old single unemployed Hispanic man had been socially withdrawn, blunted in affect, and thought disordered since his early teenage years.  He was intermittently delusional with auditory hallucinations which responded to phenothiazines.  He was treated in a day hospital after one of multiple hospitalizations; depot fluphenazine was used because of medication noncompliance.  He received two injections of 25 mg of fluphenazine decanoate separated by 1 week, with noticeable improvement in his psychotic symptoms.  He also developed akathisia and was prescribed trihexyphenadyl, 2 mg twice a day, which he probably did not take.  There was no improvement in his akathisia and no anticholinergic side effects.  He soon stopped attending the day hospital and a family member called a week later to say that the man had killed himself by jumping off the roof of their building.  He had given no indication of being suicidal and his family believed the increased ‘nervousness’ had driven him to this desperate measure.  The patient had no previous history of suicidal behavior and did not drink alcohol or use drugs.”

So, we have a young man who has been socially withdrawn and joyless since his early teens.  Not surprisingly his perceptions and thinking patterns deviated from the conventional.  For reasons unknown he came within the orbit of psychiatry, and had had extensive contact with the psychiatric system.  He was given two depot injections of fluphenazine one week apart.  His “psychotic symptoms” improved, but he developed akathisia.  He was prescribed an anticholinergic agent to combat the akathisia, but apparently this was ineffective, or as the authors suggest, he didn’t take it.  In any event, a week later he killed himself by jumping from the roof of a building.

We don’t know if the fluphenazine was administered involuntarily, but we do know that he had taken phenothiazine in the past and had been noncompliant.  So it is reasonable to assume that there was some adverse effect.  Did the day hospital psychiatrists explore the reason for this “noncompliance”?  In any event, given the outcome, the phrase “depot fluphenazine was used because of medication noncompliance” is a haunting and compelling testament to psychiatric arrogance.  This anonymous young man was clearly prone to acute akathisia, and his “noncompliance” was a sensible and correct response to the neuro-poisoning he was receiving from psychiatrists.  He stopped attending the day hospital (again, understandably),but he had no way to get the drug out of his body.  The trihexyphenidyl is an anticholinergic agent and might have mitigated the akathisia.  Or perhaps he took it and it was not effective, as is frequently the case.

“Case 2

A 36-year-old non-English speaking Hispanic man was seen once in our walk-in clinic because of severe restlessness and leg cramps.  Intermittent somatic symptoms and nervousness began shortly after he arrived in the United States 8 months earlier.  When the symptoms worsened, he began a series of visits to hospital emergency rooms and private psychiatrists.  Three weeks before the walk-in visit a Spanish-speaking psychiatrist diagnosed paranoid schizophrenia and administered depot fluphenazine.  Following this injection, the patient developed a dystonic reaction and then began to complain continuously of leg cramps and restlessness.  In the ensuing weeks he received numerous drugs from emergency room or private physicians, some given by injection and some by prescription.  He brought bottles of thiothixene, chlorazepate, amitriptyline, meprobamate, and lorazepam to the clinic.  He was agitated, paced, and begged for help.  He denied symptoms of depression or suicidal ideation.  He claimed he was devoted to his wife and 9-year-old daughter, but he felt his unbearable symptoms would never go away.  He made good contact in a translated interview and showed no thought disorder, hallucinations, or delusions.  Thorough medical examination was negative except for the parkinsonian symptoms.  He had no prior history of psychiatric treatment and the family history was negative for depression, nervousness, and significant psychiatric or medical illness.  Since the diagnosis was uncertain, plans were made to discontinue all medication and a follow-up appointment was scheduled.  The next day he killed himself without warning by jumping in front of a subway train.”

The 36-year-old man had come to the US eight months earlier, and had begun to experience “somatic symptoms and nervousness”.  This seems hardly surprising in someone who is having to adapt to a new environment, but we are provided no details with regards to his psychosocial context, other than the fact that he had a wife and 9-year-old daughter, and that he didn’t speak English.  What we do know is that he visited “emergency rooms and private psychiatrists” to help with “somatic symptoms and nervousness”.  One of the psychiatrists “diagnosed paranoid schizophrenia”, and gave him a depot injection of fluphenazine.  He developed severe akathisia, and continued to visit emergency rooms and private psychiatrists in an attempt to gain some relief.  During this period he received “numerous drugs” from these sources, some by injection, some by prescription.  At this point he came to the authors’ walk-in clinic.

“He was agitated, paced, and begged for help.”


“He denied symptoms of depression or suicidal ideation.  He claimed he was devoted to his wife and 9-year-old daughter, but he felt his unbearable symptoms would never go away.”

Plans were made to discontinue all the drugs, which the authors euphemistically refer to as medications, but it was too little, too late.  He jumped to his death in front of a train the next day.

So, we have a healthy young man, devoted to his wife and daughter, who seeks medical help for what were probably stress-related “somatic complaints and nervousness”.  Psychiatrists throw a bewildering array of drugs at him, including a depot injection of fluphenazine, which results in his death.  And the only reason we know about this forgotten victim of psychiatry is because the authors wrote up and published the case.  How many other thousands have died from the same kind of irresponsible drug-pushing; from the same arrogant conviction that for every human problem, psychiatry has a “safe and effective” pill?

. . . . . . . . . . . . . . . .

Here are some more quotes from the Shear et al article:

“Akathisia is an intensely unpleasant feeling characterized by muscle discomfort, inability to sit still, continuous agitation, restlessness, and fidgety feelings.  Sleep may be disturbed by an inability to lie down.  Some patients say they feel like jumping out of their skin”

“The estimated incidence of akathisia with neuroleptic use ranges from 20 to 45%.  Several studies using depot fluphenazine report an incidence around 35%.”

“Akathisia is a distressing  symptom which may be difficult to diagnose and treat.  Restlessness may be mistaken for anxiety and clinicians may err by raising neuroleptic dosage.”

“Sometimes the only effective treatment is withdrawal of the neuroleptic.  Although we cannot be sure that akathisia caused the deaths of our patients, akathitic symptoms seemed to be immediate precipitants of suicidal behavior.   We urge clinicians to be alert to the discomfort of akathisia and to treat it aggressively.  If treatment with anticholinergics or γ-aminobutyric acid agonists fails or symptoms are especially severe, hospitalization may be indicated.”

It is clear that the authors are leaning heavily towards the conclusion that neuroleptic-induced akathisia was the immediate precipitant of both suicides.


Several similar reports have appeared in the literature for decades.  Here are some examples, with relevant quotes:

Van Putten, T., MD, The Many Faces of Akathisia, Comprehensive Psychiatry, 1975, 16(1):

“AKATHISIA, a common side effect of neuroleptic therapy, is an emotional state and ‘refers not to any type or pattern of movement, but rather to a subjective need or desire to move.'”

“A 44-year-old woman with hebephrenic schizophrenia started to bang her head against the wall three days after an injection of 25 mg of fluphenazine enanthate.  Her only utterance was: ‘I just want to get rid of this whole body.'”

“Akathisia is often associated with strong affects of fright, terror, anger or rage, anxiety, and vague somatic complaints.”

“On this regime, she usually developed an episode of akathisia during the week following her injection.  She described several such episodes as follows: ‘I just get these attacks of tension.  I don’t feel right.  My stomach feels strange.  It’s like I’m churning inside.  I feel hostile and I hate (with intense affect) everybody.”

“Patients have described the inner restlessness and agitation of akathisia in many other ways, such as:  ‘My nerves are just jumping’ I feel like I’m wired to the ceiling; I just feel impatient and nasty.  I can’t concentrate; it’s like I got ants in my pants; my nerves are raw; I just feel on edge; I feel just nasty; I feel like jumping out of my skin; if this feeling continues, I would rather be dead.  I can’t describe the feelings; I’m quivery from the waist up; I want to climb the walls; I feel all revved up; it’s like I got diaper rash inside.'”

“Patients with severe akathisia, however, cannot sit quietly for more than a few seconds at a time, and at times the ‘impatience musculaire’ can result in running, agitated dancing, or rocking.”

“Akathisia is tolerated very poorly by hostile paranoid patients in that they tend to misinterpret the inner agitation of akathisia as further proof that they are being poisoned or controlled by outside malevolent forces.”

Note the presumably unintended irony in the word misinterpret.  In reality, they are being poisoned and controlled by outside forces!

. . . . . . . . . . . . . . . . .

Keckich, W., MD:  Neuroleptics: Violence as a Manifestation of Akathisia, JAMA, 1978, Nov 10 (240) 20, 2185:

“NEUROLEPTIC medications (eg, phenothiazines, butyrophenones) are used in medicine to control psychotic symptoms and concomitant agitated and violent behavior. They also are used to control anxiety and agitation whenever minor tranquilizers (eg, benzodiazepines) would be inappropriate. Development of akathisia as a parkinsonian side effect is confirmed in the use of these drugs.  Akathisia is a condition that gives rise to the subjective desire to be in constant motion, with a feeling of inner agitation and muscle tension. The patient cannot sit still and paces constantly”

“One week later the patient reported that he was more agitated at night.  Since it was not known at the time that akathisia was beginning, haloperidol treatment was increased to 4 mg at bedtime to decrease the agitation. Four days later, after his evening dose of 4 mg of haloperidol, he became uncontrollably agitated, could not sit still, and paced for several hours.  He complained of tightness in his muscles, rigidity, a jumpy feeling inside, and violent urges to assault anyone near him.  This culminated in an assault on his dog with an intent to kill.  He became frightened over his loss of control and came to the emergency room.  He was given 50 mg of thioridazine hydrochloride, which brought the hostility under control but did not remove it.

He subsequently discontinued the treatment with imipramine and haloperidol.  The following morning he reported that the muscle tightness, jumpy feelings, and hostility were decreased but still present.  Three days after drug treatment was discontinued all of the symptoms had ceased, and he was at his baseline of difficulty once again.  The half-life of haloperidol is approximately 24 hours, and this symptom relief coincided with expected excretion of the drug.

In retrospect it was apparent that he had experienced increasing akathitic side effects from the haloperidol medication, which accounted for his increasing night-time agitation and culminated in a stimulation of violent and aggressive activity.”

. . . . . . . . . . . . . . . .

Schulte, JL, MD, Homicide and Suicide Associated with Akathisia and Haloperidol, American Journal of Forensic Psychiatry, Jan 1985, 6(2):

“The following five cases are reported to bring attention to the potential for severe violence, as a result of akathisia, following such administration of a neuroleptic for acute psychiatric symptoms.  Particular emphasis is directed to an experience of sensory dissociation associated with the uncomfortable physical reactions, resulting in extreme acts of physical violence.”


“A 23-year-old married, Salvadorian-born male, with a four-day history of progressive paranoia and disorganized behavior, had been taken by the police department to a hospital at the request of his parents.  The physician insisted he receive an injection of haloperidol in the emergency room while awaiting admission to the psychiatric unit where he had previously been a patient on a number of occasions.

  He tried to resist but felt he had no option with the staff and police surrounding him.  He felt he was being unnecessarily delayed in being admitted to the inpatient unit.  In addition, he felt he had been lied to, in that apparently he had been told he was going to see his wife who had deserted him approximately 48 hours earlier.  He then escaped from the emergency room and the authorities, ran several miles to a park, tried to get a policeman to help him, escaped again and totally disrobed.  Within the next 45-minute period of time, he assaulted one woman who was walking her dog and attempted to rape her.  When pulled off by the husband, he proceeded down the street, broke down the front door of a house where an 81-year-old lady was sleeping.  He severely beat her with his fists, ‘to a pulp’, by his own description.  Following which he found knives and stabbed her repeatedly, resulting in her death.  Then, after being confronted in the street by a policeman who sprayed him with Mace, he returned through the house, exiting the back door where he ran into another woman with her child.  He repeatedly stabbed the woman in front of the child, whereupon he moved on to the next person he encountered, a woman whom he severely assaulted and stabbed to the extent that an eye was lost and an opening into the anus was created resulting in major surgery and serious residual problems, including a colostomy.  He was then finally captured and subdued by eight policemen and hospitalized.

He had ten previous psychiatric hospitalizations between 1975 and the present.  All of these hospitalizations have been only a matter of hours to several days.  He would always be placed on medication and released, following which he would stop taking the medication and go along until another upheaval would occur.

He had a history of problems with anger and acute paranoid beliefs leading to hyperactive behavior and one incident in which it was reported he tried to choke one of his brothers.

His description of his mental status at the time of his offense is quite striking.  He describes himself as feeling almost like a spectator in a movie.  He makes a point of describing how he had lost all sense of caring about anything or anyone in life.  Additionally, he describes a feeling of loss of physical sensation, including feeling nothing when maced by the police.  He felt enormous energy with a feeling of needing to rid himself of it.

He gives the history of having been picked up by the police on a traffic violation in 1979 and placed in jail for the first time in his life.  He became angry and was given a series of haloperidol injections, becoming progressively more agitated and unmanageable to the point he was rolled up in a mattress and handcuffed in order to be transported to a psychiatric inpatient unit.  In 1980, during another hospitalization, he was, despite his protests, changed from chlorpromazine to haloperidol and within hours became totally unmanageable, requiring six individuals to subdue him and place him in seclusion and restraint.” [Emphasis added]

It is noteworthy that this individual asked not to be changed from chlorpromazine to haloperidol, but his request was ignored.

Eight years later, Herrera et al confirmed in a controlled study that an increase in violent behavior was more likely with haloperidol than with chlorpromazine.  Apparently, the individual had some intuitive awareness of this from previous experience, but as is often the case, the psychiatrists discounted his protests and gave him the haloperidol anyway.

Here are two quotes from the Herrera et al study:

“We found in a controlled study that some patients have a marked increase in violence when treated with moderately high-dose haloperidol.”

“…these patients did not show an increase in violence during a placebo period, nor did they have a history of violent behavior.”

Back to the Schulte JL article:


“A 30-year-old man with a history of mental illness dating back seven years, with hospitalizations in three other states, was admitted to the hospital on six counts of burglary. His diagnosis was paranoid schizophrenia, and he had been found not guilty by reason of insanity by the courts. The admission note by the psychiatrist stated, ‘He is somewhat paranoid, but says he has side effects from most tranquilizers.’ On the third day of hospitalization, he was referred to the psychiatrist by nurses because of difficulty getting to sleep. No evidence of aggressiveness or self-injurious behavior was charted that day in the nurses’ notes.  The psychiatrist prescribed haloperidol, 5mg. three times a day, which was begun the next day, with three doses administered with Cogentin, 2mg twice a day. Nurses’ notes that day stated, ‘He was very anxious about being in the hospital and threatened to kill himself if he gets up the nerve.’ At 10:45 p.m., notes stated, ‘He has regressed during this shift in all assessment areas. His hygiene is poor, and he is irresponsible, e.g., lying on the floor without shoes or socks.’  He refused medication initially at 5 p. m., and stated that phenothiazines, ‘fuck me up.’  He finally took the medication but then stated angrily, ‘Now I’ll  really get crazy.’  He ranted loudly and profanely for 30 minutes. He took his 9 p.m. medication and started his haranguing again, only louder and more threatening. ‘l’ll kill all of you mother-fuckers before I leave here,’  He was found in his room at 6:50 a.m., having hung himself with a bed sheet. A letter from his attorney to the hospital had stated that ‘medications caused him problems (l should perhaps state that by medications I mean psychotropic drugs).'” [Emphasis added]


“A 52-year-old male first came to psychiatric attention eleven years earlier following an assault on his wife. He had delusions of cancer, a belief he would die and felt sexually inadequate.

He had been unsuccessfully treated with Lithium and antidepressants, as well as various tranquilizers. He had continually been an inpatient or in board and care facilities, and three and one-half months earlier, he had his medications changed to 10mg. of Haloperidol in the a.m. and 40mg. of Haloperidol at hour of sleep, with 2mg.of Artane twice daily. Each month he stated he complained to his psychiatrist of severe restlessness. He stated he had to roll over and over in bed at night and usually would be unable to get to sleep until 3 or 4 a.m. During the day, he would try to lie down but couldn’t because of his severe uncomfortableness. He described after being turned down again by the psychiatrist, he became despondent and angry, lost hope and decided if he could not ever even sleep like the rest of his boarding home mates that life wasn’t worthwhile.  He secured a knife and repeatedly stabbed himself in the abdomen, was rushed to the hospital and barely survived.  He remarked he could never even feel the knife when stabbing himself.” [Emphasis added]

. . . . . . . . . . . . . . . .

Van Putten, T. MD and Marder, SR, MD, Behavioral Toxicity of Antipsychotic Drugs, J Clin Psychiatry, September 1987, 48: 9 (Suppl):

“The subjective restlessness of akathisia is usually accompanied by telltale foot movements: rocking from foot to foot while standing or walking on the spot. Akathisia is strongly associated with depression and dysphoric responses to neuroleptics and has even been linked to suicidal and homicidal behavior in extreme cases.”

“The aforementioned case literature reads convincingly:  it is reasonable to conclude that akathisia, in the extreme case, can drive people to suicide or homicide.”

. . . . . . . . . . . . . . . .

Crowner, ML, Douyon, R, et al, Akathisia and violence Psychopharmacology Bulletin, 1990: 26(1): 115-7:

“Akathisia is a common side effect of neuroleptic drugs that may present with behavioral disturbances. There have been preliminary reports on the association between violence and akathisia. We report the first observational study of this relationship. Patients studied were from a special unit for violent patients. A closed-circuit television camera was installed in each of the corners in its dayroom. Incidents of assault plus the 5 minutes preceding each assault were recorded on videotape. Participants and bystanders were rated for the motor component of akathisia. For each of nine incidents, we compared the akathisia scores for participants and for bystanders. Both victims and assailants were akathisic before about half of all incidents; bystanders rarely were. The classification of the movements we rated and the implications for further studies are discussed.”

The extraordinary irony here is that the individuals in this study “were from a special unit for violent patients,” but in fact the drug used to control this behavior was actually precipitating more violence!

. . . . . . . . . . . . . . . .

Galynker, I, MD, PhD and Nazarian, D, MD, letter to the editor, Journal of Clinical Psychiatry, 1997, 58: 31-32:

“Case ReportMr. A, a 47-year-old white man with a diagnosis of bipolar mood disorder, was brought to the emergency room because he was screaming in the streets.  Mr. A had over 30 past psychiatric admissions associated with agitation and violence and was often discharged against medical advice.  He was nearly always noncompliant with his antipsychotic medications, claiming that they made him ‘jump and lose my temper.’  Prior to the present admission, Mr. A’s daily medications included haloperidol 20 mg, lithium carbonate 1500 mg, divalproex sodium 500 mg, and benztropine 1 mg.  At admission, the patient was grandiose, had loud and pressured speech, and admitted he was not taking haloperidol.  He was given haloperidol 15 mg q.h.s. and benztropine 1 mg q.a.m.  Within 24 hours he started pacing; became restless, agitated, and violent; complained of feeling ‘jumpy’; and attacked a staff member.  On Day 5 of his hospitalization, haloperidol and benztropine were discontinued; chlorpromazine was started, and the dose was increased to 950 mg/day.  Mr. A, although sedated, remained threatening and violent.  On Day 13, chlorpromazine was discontinued, and haloperidol was restarted at a higher dose of 15 mg p.o. b.i.d.  Mr. A again complained of ‘jumpiness’ and punched a television cabinet, causing a self-inflicted fracture.  On hospital Day 17, owing to an error, haloperidol was discontinued.  The patient became calmer, less irritable, displayed no angry outbursts, and required no further room restrictions.  After 5 days, when the error was discovered, haloperidol was restarted at a lower daily dose of 10 mg.  Within 3 days, the patient became violent and required room restriction.  Haloperidol was then discontinued, the patient’s agitation and violence resolved, and a week later he was discharged.  His daily medications were lithium carbonate 1500 mg (serum level = 0.9mEq/L; this dose had not been changed during his hospitalization), lorazepam 1 mg, and divalproex sodium 500 mg.  On these mediations, he remained well 6 months postdischarge, his longest period as an outpatient.”

In their commentary, the authors point out:

“The fact that the jumpiness occurred with haloperidol and not with chlorpromazine is another factor indicative that Mr. A has exhibited akathisia rather than nonspecific activation of mania; this is because akathisia is more common with higher potency as compared with low-potency neuroleptics.”

and, with more candor than one customarily finds in psychiatry:

“One can also speculate that Mr. A’s rocky clinical history was related to aggressive behavior perpetuated by antipsychotic administration.”

And it is worth remembering that Mr. A’s “rocky clinical history” entailed “over 30 past psychiatric admissions associated with agitation and violence”.

. . . . . . . . . . . . . . . .

So, since at least the early 80’s, individual psychiatrists have been drawing attention to the fact that neuroleptic drugs induce akathisia in many cases, and that in some cases this can precipitate suicide and/or homicide.


Although it is well known that neuroleptic drugs cause akathisia, the link between antidepressants and this condition is less widely appreciated.  The Wikipedia article on akathisia contains this:

“Antidepressants can also induce the appearance of akathisia, due to increased serotonin signalling within the CNS.”

. . . . . . . . . . . . . . . .

Hamilton, MS, MD, Obler, LA, Akathisia, suicidality, and fluoxetine, J Clin Psychiatry, 1992, Nov 53(11), 401-406, write:

“The propose[d] link between fluoxetine and suicidal ideation is explained by fluoxetine-induced akathisia and other dysphoric extrapyramidal reactions.”


“The literature suggests that fluoxetine-induced extrapyramidal reactions may be a mediator of de novo suicidal ideation.”

Fluoxetine is an SSRI, marketed as Prozac, Sarafem, and other names.

. . . . . . . . . . . . . . . .

Wirshing, WC, MD, Van Putten, T, MD, Rosenberg, J, MD, et al, Fluoxetine, Akathisia, and Suicidality: Is There a Causal Connection?, Arch Gen Psychiatry, 1992, 49(7), 580-581, write:

“We have now had experience with five such patients.  All were women.  None had a history of significant suicidal behavior; all described their distress as an intense and novel somatic-emotional state; all reported an urge to pace that paralleled the intensity of the distress; all experienced suicidal thoughts at the peak of their restless agitation; and all experienced a remission of their agitation, restlessness, pacing urge, and suicidality after the fluoxetine was discontinued. We describe herein five cases of what we think might be fluoxetine-induced akathisia accounting for suicidal ideation.”

Eikelenboom-Schieveld, SJM, Lucire, Y, MD, Fogleman, J, PhD, The relevance of cytochrome P450 polymorphism in forensic medicine and akathisia-related violence and suicide, Journal of Forensic and legal Medicine, 2016, 41. 65-71, wrote:

“Antidepressants have been reported as causing suicide and homicide and share the class attribute of frequently producing akathisia, a state of severe restlessness associated with thoughts of death and violence.”


“In this paper, we report our investigation into adverse drug reactions/interactions in three persons who committed homicide, two also intending suicide, while on antidepressants prescribed for stressful life events”


“Three persons committed homicide, two of which intended to commit suicide. None had been aggressive or mentally ill before getting medication. None had known that they needed to take medication regularly or how to stop taking it safely. None improved on medication, and no prescriber recognized their complaints as adverse drug reactions or was aware of impending danger. Interviews elicited accounts of restlessness, akathisia, confusion, delirium, euphoria, extreme anxiety, obsessive preoccupation with aggression, and incomplete recall of events. Weird impulses to kill were acted on without warning. On recovery, all recognized their actions to be out of character, and their beliefs and behaviours horrified them.”

. . . . . . . . . . . . . . . .

Whitehead, PD, Causality and Collateral Estoppel: Process and Content of Recent SSRI Litigation, 2003, J Am Acad Psychiatry Law 31:377–82, wrote:

“In Tobin v. SmithKline Beecham Pharmaceuticals a jury in the U.S. District Court for the District of Wyoming found that the medication Paxil ‘can cause some individuals to commit homicide and/or suicide,’ and that it was a legal cause of the deaths in this case.”

. . . . . . . . . . . . . . . .

Breggin, PR, MD, Suicidality, violence and mania caused by selective serotonin reuptake inhibitors (SSRIs): A review and analysis. International Journal of Risk & Safety in Medicine, 2004, 16, 31-49, wrote:

“Evidence from many sources confirms that selective serotonin reuptake inhibitors (SSRIs) commonly cause or exacerbate a wide range of abnormal mental and behavioral conditions. These adverse drug reactions include the following overlapping clinical phenomena: a stimulant profile that ranges from mild agitation to manic psychoses, agitated depression, obsessive preoccupations that are alien or uncharacteristic of the individual, and akathisia. Each of these reactions can worsen the individual’s mental condition and can result in suicidality, violence, and other forms of extreme abnormal behavior.  Evidence for these reactions is found in clinical reports, controlled clinical trials, and epidemiological studies in children and adults. Recognition of these adverse drug reactions and withdrawal from the offending drugs can prevent misdiagnosis and the worsening of potentially severe iatrogenic disorders. These findings also have forensic application in criminal, malpractice, and product liability cases.”


“There are many reports and studies confirming that SSRI antidepressants can cause violence, suicide, mania and other forms of psychotic and bizarre behavior.”

. . . . . . . . . . . . . . . .

Although there is a great deal of prima facie evidence and many case reports detailing the neuroleptic/antidepressant link to suicide and violence, there has not to my knowledge been a definitive large-scale study by American psychiatry of the link between psychiatric drugs and the murder/suicides that are occurring with increased frequency.

And the great question is:  why not?  Why is this urgent, life-threatening issue not afforded the highest priority by the APA, NIMH, and university psychiatry departments?  Is their self-serving need to protect psychiatry from the consequences of its errors eclipsing their ethical integrity and their sense of responsibility?


In this regard, it’s interesting to see how psychiatric drug-induced akathisia has been handled in the various editions of DSM.

DSM-III-R (1987) makes no specific reference to neuroleptic or antidepressant-induced akathisia.  There are, however, a number of statements in the chapter on “schizophrenia” which clearly (and deceptively) ascribe symptoms of akathisia and tardive dyskinesia to “schizophrenia” itself.  For instance:

“In addition, odd mannerisms, grimacing, or waxy flexibility may be present [in schizophrenia]. (p 190)

“Almost any symptom can occur as an associated feature [of schizophrenia].  The person may appear perplexed, disheveled, or eccentrically groomed or dressed. Abnormalities of psychomotor activity—e.g., pacing, rocking, or apathetic immobility—are common.” (p 190) [Emphasis added]

In reality, most of the pacing, grimacing, and rocking exhibited by people labeled schizophrenic is a direct result of neuroleptic drug poisoning, and not an associated feature of the so-called illness itself.

“Dysphoric mood is common [with schizophrenia], and may take the form of depression, anxiety, anger, or a mixture of these.” (p 190)

Anxiety and anger are also direct effects of neuroleptic poisoning for many people.

“Although violent acts performed by people with this disorder often attract public attention, whether their frequency is actually greater  than in the general population is not known.  What is known is that the life expectancy of people with Schizophrenia is shorter than that of the general population because of an increased suicide rate and death from a variety of other causes.” (p 191)

As is clear from the material quoted earlier, suicide is frequently a result of akathisia.  The phrase “death from a variety of other causes” is unclear.

. . . . . . . . . . . . . . . . 

DSM-IV (1994) was markedly more honest in acknowledging the existence of neuroleptic-induced akathisia.  In fact, this was included as an actual diagnosis in the fourth edition.  It was coded as 333.99, and 2½ pages (744-746) were devoted to its description.  Here are some quotes:

“In its most severe form, the individual may be unable to maintain any position for more than a few seconds.” (p 744)

“The subjective distress resulting from akathisia is significant and can lead to noncompliance with neuroleptic treatment.  Akathisia may be associated with dysphoria, irritability, aggression, or suicide attempts.  Worsening of psychotic symptoms or behavioral dyscontrol may lead to an increase in neuroleptic medication dose, which may exacerbate the problem.  Akathisia can develop very rapidly after initiating or increasing neuroleptic medication.  The development of akathisia appears to be dose dependent and to be more frequently associated with particular neuroleptic medications.  Acute akathisia tends to persist for as long as neuroleptic medications are continued, although the intensity may fluctuate over time.  The reported prevalence of akathisia among individuals receiving neuroleptic medication has varied widely (20%-75%).” (p 745) [Emphasis added]

Note the reference in the third line above to “irritability, aggression, or suicide attempts“.  In fact, as the material quoted earlier makes clear, neuroleptic-induced akathisia has been causally-linked to actual homicides and suicides.  This understatement was clearly deliberate, as Allen Frances, MD, architect of DSM-IV, was also one of the authors of the Shear et al paper quoted earlier, which linked neuroleptic-induced akathisia to actual completed suicides.

“Neuroleptic-Induced Acute Akathisia may be clinically indistinguishable from syndromes of restlessness due to certain neurological or other general medical conditions, to nonneuroleptic substances, and to agitation presenting as part of a mental disorder (e.g., a Manic Episode).” (p 745)

In other words, people who are experiencing neuroleptic-induced acute akathisia are at risk of being assigned a “diagnosis” of “bipolar disorder”!

Serotonin-specific reuptake inhibitor antidepressant medications may produce  akathisia that appears to be identical in phenomenology and treatment response to Neuroleptic-Induced Acute Akathisia.  Akathisia due to nonneuroleptic medication can be diagnosed as Medication-Induced Movement Disorder Not Otherwise Specified.” (p 745) [Bold face in original]


“Individuals with Depressive Episodes, Manic Episodes, Generalized Anxiety Disorder, Schizophrenia and other Psychotic Disorders, Attention-Deficit/Hyperactivity Disorder, dementia, delirium, Substance Intoxication, (e.g., with cocaine), or Substance Withdrawal (.e.g., from an opioid) may also display agitation that is difficult to distinguish from akathisia.” (p 745-746) [Bold face in original]

Which prompts one to wonder how many people who have been assigned these so-called diagnoses were actually suffering from one of the toxic effects of neuroleptic drugs or SSRI’s.  It is also entirely plausible, as DSM-IV suggests, that many of these individuals would have been “treated” with even higher doses of neuroleptics!

. . . . . . . . . . . . . . . .

The entry in DSM-IV-TR (2000) is identical to that in DSM-IV except for the following addition:

“Although the atypical [newer] neuroleptic medications are less likely to cause akathisia than the typical [older] neuroleptics, nonetheless, these medications do cause akathisia in some individuals.” (p 801)

. . . . . . . . . . . . . . . . .

DSM-5 is remarkably less frank concerning psychiatric drug-induced akathisia than was DSM-IV.  The name Neuroleptic-Induced Acute Akathisia was changed to Medication-Induced Acute Akathisia and the entry is given a total of four-and-a-half lines of text:

333.99 (G25.71)  Medication-Induced Acute Akathisia
Subjective complaints of restlessness, often accompanied by observed excessive movements (e.g., fidgety movements of the legs, rocking from foot to foot, pacing, inability to sit or stand still), developing within a few weeks of starting or raising the dosage of a medication (such as a neuroleptic) or after reducing the dosage of a medication used to treat extrapyramidal symptoms.” (p 711) [Bold face in original]

There is no reference to the fact that, as earlier psychiatric authors had stated, the condition can be so unbearable as to drive people to suicide and even homicide.

There is, however, an interesting admission in a separate, also brief, entry:

“333.72 (G24.09)  Tardive Dystonia
 333.99  (G25.71)  Tardive Akathisia
Tardive syndrome involving other types of movement problems, such as dystonia or akathisia, which are distinguished by their late emergence in the course of treatment and their potential persistence for months to years, even in the face of neuroleptic discontinuation or dosage reduction.” (p 712) [Bold face in original]

In other words, neuroleptic-induced akathisia can persist for years, even if the person stops taking the drugs!  But even granting this admission, it is clear that DSM-5 is markedly down-playing the significance and seriousness of neuroleptic-induced akathisia.  And it is also clear from elsewhere in the text that the agenda here is to protect the reputation of the neuroleptic drugs:

“The term neuroleptic is becoming outdated because it highlights the propensity of antipsychotic medications to cause abnormal movements, and it is being replaced with the term antipsychotic in many contexts.” (p 709)

Note the deceptive use of the passive voice (“is becoming outdated”).  In reality, psychiatrists are consciously and deliberately phasing out the term “neuroleptic” in an attempt to conceal, or at least not draw attention to, the severe and potentially life-threatening neurotoxic effects of these drugs.

But the more important question is why has the APA eliminated the DSM-IV category “neuroleptic-induced akathisia” that ran to 2 ½ pages, and replaced it with the more general “medication-induced acute akathisia”, which runs to 4 ½ lines?  Why has this dangerous and relatively widespread adverse effect been so downplayed?  On page 809 of the DSM-5 text there is a section called Highlights of Changes from DSM-IV to DSM-5, but there is no explanation for the change there.  There is a note in this section referring the reader to “An expanded description of nearly all changes…” on the APA website.  The link leads to an article titled “Highlights of Changes from DSM-IV-TR to DSM-5“.  But the article contains no reference to the change in question.

So we don’t know the APA’s justification for suppressing information about this potentially devastating adverse effect.  But we do know that neuroleptic drugs are being prescribed for an increasing range of problems, and are even being prescribed to toddlers for temper tantrums and to nursing home residents for “management problems”.  Some have even acquired “block-buster” sales status.  It is clearly in pharma’s interests to suppress this information and it is consistent with psychiatry’s hand-in-glove relationship with pharma that they should oblige their generous benefactors in this way.  Remember, 69% of the DSM-5 workforce were in the pay of pharma while working on the revision.

Despite the early, and very clear, statements from individual psychiatrists linking psychiatric drugs to murder/suicides, the psychiatric leadership has consistently failed to address this link.  Instead, they deceptively attribute these incidents to a lack of psychiatric “treatment”, and they call for legal enforcement of even more drugging.


On June 9, 2016, Maria Oquendo, MD, President of the APA, wrote a post in support of the Senate’s so-called Mental Health Reform Bill.  The post was standard psychiatric propaganda, including the inane 21% annual and 50% lifetime prevalence of “mental illness”.  The reality is that if one can invent illnesses at will and arbitrarily reduce the “diagnostic” thresholds of these “illnesses”, one can produce any prevalence numbers one chooses.

The post also drew attention to the fact that there were 41,000 suicides in the US in 2013, and asserted that “…we continue to fail people with mental illness every day.”

In other words, more psychiatric treatment would reduce the suicide rate.  But meanwhile, we have no data on how many of these individuals were in the throes of neuroleptic or antidepressant-induced akathisia.  And as long as psychiatry and pharma are controlling the research agenda, such information will be systematically repressed.

As I’ve stated many times, psychiatry is intellectually and morally bankrupt.  They are adamantly resistant to anything resembling critical self-appraisal, and there are no depths of deception and spin to which they will not go, to suppress the reality and the consequences of their drug-pushing depredations.  Neuroleptic and antidepressant drugs induce some individuals to take their own lives and/or the lives of others.  Neuroleptic and antidepressant drugs are almost certainly the proximate causes of many of the mass shootings that have plagued our country for almost twenty years.  How much longer can psychiatry sustain this dreadful, self-serving deception?


Senator John McCain and Congressman David Jolly have introduced bills in their respective chambers that if enacted will require the Veterans Administration to conduct a comprehensive study of the link between psychiatric drugs and veterans’ suicides.  It will be an enormous step forward if these bills become law.  It is also an interesting reflection that these bills were initiated by politicians, and not by psychiatrists, who present themselves as caring professionals acting in the best interests of their so-called patients.

If you live in the US, please encourage your representatives to support the McCain and Jolly bills (S 3410 and H 4640).

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.


Melissa, a commenter on a recent post, asked if I would do a post on akathisia.

Akathisia literally means inability to sit.  People with this problem typically pace for long periods, and if they do sit down, they continue to keep moving and shifting their position in the chair.

In severity it can range from a generalized sense of uneasiness or agitation, to severe discomfort and even pain.  The discomfort tends to be located in the legs, but can also occur in the hip and pelvic area.  In severe cases, the victims pace to the point of exhaustion, but even then sitting does not relieve the discomfort.


The major cause of akathisia is the ingestion of neuroleptics and other drugs, including SSRIs and other antidepressants.

Akathisia also occurs in withdrawal from benzodiazepines (e.g. Valium, Xanax, etc.), opiates, and amphetamines.


Akathisia is usually treated symptomatically with propranolol (Inderal), a beta-blocker widely used to treat high blood pressure.  Possible side effects include: congestive heart failure, insomnia, hallucinations, short-term memory loss, etc…

Benzodiazepines are sometimes used in the management of akathisia, but this, of course, can precipitate further problems on withdrawal.

Akathisia often stops when the drugs are discontinued, but in some cases can persist even years after the drugs are stopped.

Neuroleptic-induced akathisia is listed in DSM-IV-TR (under medication-induced movement disorders).  DSM states that “Akathisia may be associated with dysphoria, irritability, aggression or suicide attempts.” (p 801). [emphasis added]

It is widely maintained that akathisia is the “mechanism” linking SSRI’s with suicide and violence.  See, for instance, SSRI-Induced Akathisia’s Link To Suicide and Violence, by Evelyn Pringle.

It is not possible to communicate the profound horror of severe akathisia in a brief post such as this.  In the late 80’s, I worked for a while at a publicly-funded substance abuse unit in an Eastern state.  The unit was on the grounds of a state hospital, but was separate from the hospital physically and administratively.

During my lunch hour, I often walked in the grounds, and most days I encountered Betty (not her real name).  She had been resident at the hospital for years, and had extreme tardive dyskinesia and akathisia.  She was about 50, but looked more like 70.  She walked the grounds constantly in almost all weathers.  We would stop and chat, though her tardive dyskinesia made her speech almost unintelligible.  But even while she was stopped, she continued to pace on the spot.  She literally couldn’t stop.  And after a few minutes, she would move on.

I used to wonder what possible benefit outweighed the dreadful damage that had been done to this woman.  What risk had she posed to herself or to others that justified reducing her to this state of perpetual torment?

Sometimes I get tired of writing these posts; tired of sifting through the facile lies of psychiatric complacency; tired of reading about psychiatry’s fat cats wallowing in the corrupting bounty of pharma money.  And then, I remember Betty.  Poor old Betty, living as best she could in her psychiatry-fabricated Hell.

If you’ve never seen a person suffering from akathisia, there’s a video here.